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      <title>Wiley: Clinical &amp; Experimental Allergy: Table of Contents</title>
      <link>https://onlinelibrary.wiley.com/journal/13652222?af=R</link>
      <description>Table of Contents for Clinical &amp; Experimental Allergy. List of articles from both the latest and EarlyView issues.</description>
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      <pubDate>Tue, 07 Apr 2026 07:17:20 +0000</pubDate>
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      <dc:title>Wiley: Clinical &amp; Experimental Allergy: Table of Contents</dc:title>
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         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70299?af=R</link>
         <pubDate>Mon, 06 Apr 2026 20:38:20 -0700</pubDate>
         <dc:date>2026-04-06T08:38:20-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
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         <title>Does ABPA Contribute to Bronchiectasis? A Structured Evaluation of Competing Hypotheses</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Systematic evaluation of competing hypothesis suggests that ABPA contributes to bronchiectasis through antigen‐driven type‐2 immune injury in susceptible hosts.

ABSTRACT
Whether allergic bronchopulmonary aspergillosis (ABPA) causes bronchiectasis or merely represents Aspergillus fumigatus colonisation of damaged airways remains debated. Establishing causality is challenging because airway damage is predominantly driven by host immune responses rather than by direct fungal invasion. We systematically evaluate four competing hypotheses: (i) ABPA causes bronchiectasis, (ii) reverse causation, with bronchiectasis predisposing to ABPA, (iii) a shared underlying factor independently producing both conditions and (iv) a spurious association. We evaluate radiological, pathological, immunological, temporal and therapeutic evidence in relation to these hypotheses. The characteristic radiological phenotype (central bronchiectasis and high‐attenuation mucus), eosinophil‐dominant histopathology and disease‐specific immunological profile (typically absent in other forms of bronchiectasis despite Aspergillus colonisation) distinguish ABPA from incidental colonisation. Randomised controlled trials demonstrating that antifungal treatment or anti‐inflammatory therapy (glucocorticoids and biological agents) improve clinical and immunological outcomes argue against a purely spurious association. Temporal observations indicate that ABPA precedes bronchiectasis in many cases. While uncertainty remains and host susceptibility is likely essential, the available evidence suggests that ABPA contributes to bronchiectasis through antigen‐driven immune injury, supporting the use of appropriate antifungal and immunomodulatory therapy in selected patients.
</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/a6dc58e5-1a43-4dfa-b1ff-c62d711de20c/cea70299-toc-0001-m.png"
     alt="Does ABPA Contribute to Bronchiectasis? A Structured Evaluation of Competing Hypotheses"/&gt;
&lt;p&gt;Systematic evaluation of competing hypothesis suggests that ABPA contributes to bronchiectasis through antigen-driven type-2 immune injury in susceptible hosts.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Whether allergic bronchopulmonary aspergillosis (ABPA) causes bronchiectasis or merely represents &lt;i&gt;Aspergillus fumigatus&lt;/i&gt; colonisation of damaged airways remains debated. Establishing causality is challenging because airway damage is predominantly driven by host immune responses rather than by direct fungal invasion. We systematically evaluate four competing hypotheses: (i) ABPA causes bronchiectasis, (ii) reverse causation, with bronchiectasis predisposing to ABPA, (iii) a shared underlying factor independently producing both conditions and (iv) a spurious association. We evaluate radiological, pathological, immunological, temporal and therapeutic evidence in relation to these hypotheses. The characteristic radiological phenotype (central bronchiectasis and high-attenuation mucus), eosinophil-dominant histopathology and disease-specific immunological profile (typically absent in other forms of bronchiectasis despite &lt;i&gt;Aspergillus&lt;/i&gt; colonisation) distinguish ABPA from incidental colonisation. Randomised controlled trials demonstrating that antifungal treatment or anti-inflammatory therapy (glucocorticoids and biological agents) improve clinical and immunological outcomes argue against a purely spurious association. Temporal observations indicate that ABPA precedes bronchiectasis in many cases. While uncertainty remains and host susceptibility is likely essential, the available evidence suggests that ABPA contributes to bronchiectasis through antigen-driven immune injury, supporting the use of appropriate antifungal and immunomodulatory therapy in selected patients.&lt;/p&gt;</content:encoded>
         <dc:creator>
Ritesh Agarwal, 
Inderpaul Singh Sehgal, 
Valliappan Muthu, 
Philip Bardin
</dc:creator>
         <category>REVIEW ARTICLE</category>
         <dc:title>Does ABPA Contribute to Bronchiectasis? A Structured Evaluation of Competing Hypotheses</dc:title>
         <dc:identifier>10.1111/cea.70299</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70299</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70299?af=R</prism:url>
         <prism:section>REVIEW ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70266?af=R</link>
         <pubDate>Mon, 06 Apr 2026 19:47:59 -0700</pubDate>
         <dc:date>2026-04-06T07:47:59-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
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         <title>Effects of Common Food Additives Kappa‐, Iota‐ and Lambda‐Carrageenans on Intestinal Epithelial Cell Activation and Barrier Disruption</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Carrageenans, widely used food additives, disrupted intestinal epithelial integrity in a gut‐on‐a‐chip model. All types (κ‐, ɩ‐, λ‐) induced cytotoxicity, inflammation and tight junction (TJ) disruption, triggering TNF‐mediated immune responses. λ‐Carrageenan had the most severe effects, supporting the Epithelial Barrier Theory linking food additives to chronic inflammatory diseases.

ABSTRACT

Background
The epithelial barrier theory has been proposed to link the onset of many chronic inflammatory diseases to the damaged epithelial barrier induced by numerous environmental factors, including food emulsifiers. This study aimed to investigate the effects of food emulsifiers kappa‐, iota‐ and lambda‐carrageenan on intestinal epithelial barrier integrity and the underlying mechanisms.


Methods
The cytotoxicity and apoptosis of carrageenans were determined using Hoechst/propidium iodide staining and FITC annexin V/propidium iodide staining, respectively. The gut‐on‐a‐chip was established and transepithelial electrical resistance measurement, paracellular flux assay, immunofluorescence staining of tight junction proteins, RNA‐sequencing and targeted proteomics were performed.


Results
Kappa‐, iota‐ and lambda‐carrageenans induced dose‐dependent cytotoxicity, with lambda‐carrageenan showing a more severe cytotoxic effect in relatively lower doses. All three carrageenans elicited a dose‐ and time‐dependent decrease of gut epithelial barrier strength, a significant increase in the paracellular flux and irregular and heterogeneous staining of occludin and ZO‐1 compared to the untreated group, suggesting the disruption of the intestinal epithelial barrier integrity. Transcriptomics data revealed that iota‐ and lambda‐carrageenan induced more severe pro‐inflammatory responses, which were associated with the upregulation of genes involved in TNF signalling, IL‐17 signalling cellular response to chemokines, cholesterol metabolism and NF‐kappa B signalling pathways. Targeted proteomics data from exposed gut‐on‐a‐chips indicated an upregulation of inflammation‐ and immune response‐related proteins for all three carrageenans.


Conclusions
The present study provides direct evidence for the detrimental effects of kappa‐, iota‐ and lambda‐carrageenans on gut epithelial cell activation and barrier integrity. The underlying mechanism of epithelial barrier disruption was largely attributed to the activation of innate immune responses by carrageenans, resulting in a pro‐inflammatory response.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/5ce7363e-c645-486a-a4b0-57d51e67db1e/cea70266-toc-0001-m.png"
     alt="Effects of Common Food Additives Kappa-, Iota- and Lambda-Carrageenans on Intestinal Epithelial Cell Activation and Barrier Disruption"/&gt;
&lt;p&gt;Carrageenans, widely used food additives, disrupted intestinal epithelial integrity in a gut-on-a-chip model. All types (κ-, ɩ-, λ-) induced cytotoxicity, inflammation and tight junction (TJ) disruption, triggering TNF-mediated immune responses. λ-Carrageenan had the most severe effects, supporting the Epithelial Barrier Theory linking food additives to chronic inflammatory diseases.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;The epithelial barrier theory has been proposed to link the onset of many chronic inflammatory diseases to the damaged epithelial barrier induced by numerous environmental factors, including food emulsifiers. This study aimed to investigate the effects of food emulsifiers kappa-, iota- and lambda-carrageenan on intestinal epithelial barrier integrity and the underlying mechanisms.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;The cytotoxicity and apoptosis of carrageenans were determined using Hoechst/propidium iodide staining and FITC annexin V/propidium iodide staining, respectively. The gut-on-a-chip was established and transepithelial electrical resistance measurement, paracellular flux assay, immunofluorescence staining of tight junction proteins, RNA-sequencing and targeted proteomics were performed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Kappa-, iota- and lambda-carrageenans induced dose-dependent cytotoxicity, with lambda-carrageenan showing a more severe cytotoxic effect in relatively lower doses. All three carrageenans elicited a dose- and time-dependent decrease of gut epithelial barrier strength, a significant increase in the paracellular flux and irregular and heterogeneous staining of occludin and ZO-1 compared to the untreated group, suggesting the disruption of the intestinal epithelial barrier integrity. Transcriptomics data revealed that iota- and lambda-carrageenan induced more severe pro-inflammatory responses, which were associated with the upregulation of genes involved in TNF signalling, IL-17 signalling cellular response to chemokines, cholesterol metabolism and NF-kappa B signalling pathways. Targeted proteomics data from exposed gut-on-a-chips indicated an upregulation of inflammation- and immune response-related proteins for all three carrageenans.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;The present study provides direct evidence for the detrimental effects of kappa-, iota- and lambda-carrageenans on gut epithelial cell activation and barrier integrity. The underlying mechanism of epithelial barrier disruption was largely attributed to the activation of innate immune responses by carrageenans, resulting in a pro-inflammatory response.&lt;/p&gt;</content:encoded>
         <dc:creator>
Na Sun, 
Yagiz Pat, 
Huseyn Babayev, 
Sena Ardicli, 
Ismail Ogulur, 
Xianting Bu, 
Manru Li, 
Shuqi Jia, 
Beate Rückert, 
Raja Dhir, 
Kari C. Nadeau, 
Mubeccel Akdis, 
Cezmi A. Akdis, 
Duygu Yazici
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Effects of Common Food Additives Kappa‐, Iota‐ and Lambda‐Carrageenans on Intestinal Epithelial Cell Activation and Barrier Disruption</dc:title>
         <dc:identifier>10.1111/cea.70266</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70266</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70266?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70297?af=R</link>
         <pubDate>Mon, 06 Apr 2026 19:45:44 -0700</pubDate>
         <dc:date>2026-04-06T07:45:44-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70297</guid>
         <title>Association of Penicillin Allergy Label With Post‐COVID‐19 Condition and Subsequent Clinical Outcomes: A Population‐Based Cohort Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ubonphan Chaichana, 
Kenneth K. C. Man, 
Chengsheng Ju, 
Yogini H. Jani, 
Li Wei
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Association of Penicillin Allergy Label With Post‐COVID‐19 Condition and Subsequent Clinical Outcomes: A Population‐Based Cohort Study</dc:title>
         <dc:identifier>10.1111/cea.70297</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70297</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70297?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70288?af=R</link>
         <pubDate>Sun, 05 Apr 2026 21:10:57 -0700</pubDate>
         <dc:date>2026-04-05T09:10:57-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70288</guid>
         <title>Prevalence and Sociodemographic Variation of Allergic Diseases in Australia: Findings From the Australian National Health Survey</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Using data from 17,093 participants in the 2022 Australian National Health Survey, this study is the first to report nationwide prevalence estimates for allergic rhinitis (23.9%), food allergy (7.0%), drug allergy (5.2%), eczema (1.6%) and diagnosed asthma (10.8%) across Australia. The report shows how allergy rates vary by age, geographic region and sociodemographic characteristics.

ABSTRACT

Background
The prevalence of allergic diseases across the Australian population, in all regions and age groups, is not well documented. This study aimed to describe the prevalence and distribution of five allergic diseases (allergic rhinitis, asthma, drug allergy, eczema, and food allergy) and examine differences by sociodemographic factors.


Methods
This study used data from the 2022 cross‐sectional Australian National Health Survey. The survey randomly selected a sample of 13,095 households (with 17,093 participants) living in private dwellings in all Australian states and territories. Questionnaires were completed via face‐to‐face interviews. Allergic rhinitis, asthma, drug allergy, eczema, and food allergy were captured as self‐ or parent‐reported long‐term health conditions. Weighted estimates and relative standard errors were extracted and analysed. Prevalence was calculated using population data from the Australian 2021 Census.


Results
The prevalence of self‐reported current allergic rhinitis in Australia was 23.9% (95% CI: 23.1%–24.8%), food allergy was 7.0% (95% CI: 6.5%–7.5%), drug allergy was 5.2% (95% CI: 4.7%–5.6%), eczema was 1.6% (95% CI: 1.3%–1.9%), and diagnosed asthma was 10.8% (95% CI: 10.2%–11.5%). Food allergy and asthma prevalence were similar across childhood and adulthood, whereas the prevalence of allergic rhinitis increased sharply during early adulthood. Eczema was more common in childhood, while drug allergy was more common in later adulthood. Higher rates of allergic rhinitis, food allergy, and eczema were reported among individuals with more advantaged socio‐economic status. In general, allergic diseases were less commonly reported by Indigenous Australians compared to non‐Indigenous Australians, and by individuals born overseas compared to those born in Australia; however, prevalence varied markedly by region of birth, with some regions exhibiting higher reported rates.


Conclusions
We identified a high overall prevalence of allergic diseases in Australia, with variations across populations. The differences across populations may reflect actual prevalence or disparities in disease recognition, reporting, or access to diagnostic services.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/db8603cd-ea43-49bf-a74a-09bedfaca1e7/cea70288-toc-0001-m.png"
     alt="Prevalence and Sociodemographic Variation of Allergic Diseases in Australia: Findings From the Australian National Health Survey"/&gt;
&lt;p&gt;Using data from 17,093 participants in the 2022 Australian National Health Survey, this study is the first to report nationwide prevalence estimates for allergic rhinitis (23.9%), food allergy (7.0%), drug allergy (5.2%), eczema (1.6%) and diagnosed asthma (10.8%) across Australia. The report shows how allergy rates vary by age, geographic region and sociodemographic characteristics.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;The prevalence of allergic diseases across the Australian population, in all regions and age groups, is not well documented. This study aimed to describe the prevalence and distribution of five allergic diseases (allergic rhinitis, asthma, drug allergy, eczema, and food allergy) and examine differences by sociodemographic factors.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;This study used data from the 2022 cross-sectional Australian National Health Survey. The survey randomly selected a sample of 13,095 households (with 17,093 participants) living in private dwellings in all Australian states and territories. Questionnaires were completed via face-to-face interviews. Allergic rhinitis, asthma, drug allergy, eczema, and food allergy were captured as self- or parent-reported long-term health conditions. Weighted estimates and relative standard errors were extracted and analysed. Prevalence was calculated using population data from the Australian 2021 Census.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The prevalence of self-reported current allergic rhinitis in Australia was 23.9% (95% CI: 23.1%–24.8%), food allergy was 7.0% (95% CI: 6.5%–7.5%), drug allergy was 5.2% (95% CI: 4.7%–5.6%), eczema was 1.6% (95% CI: 1.3%–1.9%), and diagnosed asthma was 10.8% (95% CI: 10.2%–11.5%). Food allergy and asthma prevalence were similar across childhood and adulthood, whereas the prevalence of allergic rhinitis increased sharply during early adulthood. Eczema was more common in childhood, while drug allergy was more common in later adulthood. Higher rates of allergic rhinitis, food allergy, and eczema were reported among individuals with more advantaged socio-economic status. In general, allergic diseases were less commonly reported by Indigenous Australians compared to non-Indigenous Australians, and by individuals born overseas compared to those born in Australia; however, prevalence varied markedly by region of birth, with some regions exhibiting higher reported rates.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;We identified a high overall prevalence of allergic diseases in Australia, with variations across populations. The differences across populations may reflect actual prevalence or disparities in disease recognition, reporting, or access to diagnostic services.&lt;/p&gt;</content:encoded>
         <dc:creator>
Yichao Wang, 
Jennifer J. Koplin, 
Janet M. Davies, 
Constance H. Katelaris, 
Debra J. Palmer, 
Jason A. Trubiano, 
Joy Lee, 
Michaela Lucas, 
Michael O′Sullivan, 
Sandra Vale, 
Sheryl van Nunen, 
Troy Wanandy, 
Dianne E. Campbell, 
Kirsten P. Perrett, 
Rachel L. Peters
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Prevalence and Sociodemographic Variation of Allergic Diseases in Australia: Findings From the Australian National Health Survey</dc:title>
         <dc:identifier>10.1111/cea.70288</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70288</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70288?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70295?af=R</link>
         <pubDate>Thu, 02 Apr 2026 03:41:48 -0700</pubDate>
         <dc:date>2026-04-02T03:41:48-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70295</guid>
         <title>Reclassification of GST Allergens Based on Their Cross‐Reactivity in Two Divergent Cockroach Species</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Guangning Zong, 
Ana Lozano, 
Gage O. Leighton, 
Thomas Randall, 
Lars C. Pedersen, 
Jill Glesner, 
Bryan R. E. Smith, 
Nathalie Acevedo, 
Coby Schal, 
Luis Caraballo, 
Anna Pomés, 
Josefina Zakzuk, 
Geoffrey A. Mueller
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Reclassification of GST Allergens Based on Their Cross‐Reactivity in Two Divergent Cockroach Species</dc:title>
         <dc:identifier>10.1111/cea.70295</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70295</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70295?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70293?af=R</link>
         <pubDate>Tue, 31 Mar 2026 00:01:59 -0700</pubDate>
         <dc:date>2026-03-31T12:01:59-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70293</guid>
         <title>Predictive Biomarkers for Sustained Unresponsiveness Following Oral Immunotherapy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Duan Ni, 
Ralph Nanan
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Predictive Biomarkers for Sustained Unresponsiveness Following Oral Immunotherapy</dc:title>
         <dc:identifier>10.1111/cea.70293</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70293</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70293?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70291?af=R</link>
         <pubDate>Mon, 30 Mar 2026 16:18:55 -0700</pubDate>
         <dc:date>2026-03-30T04:18:55-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70291</guid>
         <title>Rebound Pruritus and Urticaria After Discontinuation of Chronic Antihistamine Use—A Scoping Review</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Rebound pruritus and urticaria have been reported after discontinuation of chronic cetirizine or levocetirizine use only. Symptoms typically occur within 0.5–5 days after stopping therapy and appear more frequently reported in female patients. Re‐initiation of antihistamines is the most commonly effective management strategy, highlighting the need for clinician awareness when discontinuing long‐term antihistamine therapy.

ABSTRACT

Background
Rebound pruritus and urticaria have been increasingly reported following discontinuation of chronic antihistamines, particularly with cetirizine and levocetirizine, prompting the United States Food and Drug Administration to issue a recent safety warning for these two medications. Currently, there are significant gaps regarding the risk factors, course and optimal management of rebound pruritus and urticaria after discontinuation of chronic antihistamine use, and if this represents a class‐specific adverse effect. This review aimed to map the literature related to rebound pruritus and urticaria after discontinuation of chronic antihistamine use.


Methods
A scoping review was conducted across four major literature databases (PubMed, Embase, Web of Science and Cochrane database) and grey literature (GreySource, OpenGrey, Google Scholar) from inception to December 2025. Articles describing rebound pruritus following discontinuation of chronic antihistamine use in paediatric or adult populations were included. Antihistamines evaluated included all first‐ and second‐generation histamine‐1 antagonists. Non‐English articles were excluded. A narrative synthesis was conducted to summarise the reported risk factors, clinical course and potential management strategies for rebound pruritus following antihistamine discontinuation.


Results
Of the 17,346 records retrieved, two retrospective studies, one case series and one case report were included in the review. The studies were conducted in the United States (n = 2), the Netherlands (n = 1) and Singapore (n = 1). The main antihistamines implicated in after discontinuation rebound pruritus were cetirizine (n = 327), levocetirizine (n = 39) and, both cetirizine and levocetirizine (n = 2). Among these patients, 85 patients experienced concomitant urticaria after discontinuation of chronic antihistamines. No report was noted for other antihistamines. The patients' age ranged from 6 to 71 years, with a female predominance (76.1%). Antihistamine use ranged from months to years, with pruritus developing between 1 to 5 days after discontinuation. Among the common treatment strategies adopted, cetirizine or levocetirizine re‐initiation was the most effective (n = 136 of 137, 99.2%), while antihistamine tapering had the lowest rate of symptoms resolution (n = 11 of 33, 33.3%).


Conclusions
Rebound pruritus following discontinuation of chronic cetirizine or levocetirizine use represents a clinically relevant adverse effect that warrants careful monitoring and management. Future research is required to identify the optimal treatment strategy and if the discontinuation of other antihistamines could also lead to rebound pruritus.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/2b1279d2-02bf-48b1-ae40-fa3679d17e75/cea70291-toc-0001-m.png"
     alt="Rebound Pruritus and Urticaria After Discontinuation of Chronic Antihistamine Use—A Scoping Review"/&gt;
&lt;p&gt;Rebound pruritus and urticaria have been reported after discontinuation of chronic cetirizine or levocetirizine use only. Symptoms typically occur within 0.5–5 days after stopping therapy and appear more frequently reported in female patients. Re-initiation of antihistamines is the most commonly effective management strategy, highlighting the need for clinician awareness when discontinuing long-term antihistamine therapy.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Rebound pruritus and urticaria have been increasingly reported following discontinuation of chronic antihistamines, particularly with cetirizine and levocetirizine, prompting the United States Food and Drug Administration to issue a recent safety warning for these two medications. Currently, there are significant gaps regarding the risk factors, course and optimal management of rebound pruritus and urticaria after discontinuation of chronic antihistamine use, and if this represents a class-specific adverse effect. This review aimed to map the literature related to rebound pruritus and urticaria after discontinuation of chronic antihistamine use.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A scoping review was conducted across four major literature databases (PubMed, Embase, Web of Science and Cochrane database) and grey literature (GreySource, OpenGrey, Google Scholar) from inception to December 2025. Articles describing rebound pruritus following discontinuation of chronic antihistamine use in paediatric or adult populations were included. Antihistamines evaluated included all first- and second-generation histamine-1 antagonists. Non-English articles were excluded. A narrative synthesis was conducted to summarise the reported risk factors, clinical course and potential management strategies for rebound pruritus following antihistamine discontinuation.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Of the 17,346 records retrieved, two retrospective studies, one case series and one case report were included in the review. The studies were conducted in the United States (&lt;i&gt;n&lt;/i&gt; = 2), the Netherlands (&lt;i&gt;n&lt;/i&gt; = 1) and Singapore (&lt;i&gt;n&lt;/i&gt; = 1). The main antihistamines implicated in after discontinuation rebound pruritus were cetirizine (&lt;i&gt;n&lt;/i&gt; = 327), levocetirizine (&lt;i&gt;n&lt;/i&gt; = 39) and, both cetirizine and levocetirizine (&lt;i&gt;n&lt;/i&gt; = 2). Among these patients, 85 patients experienced concomitant urticaria after discontinuation of chronic antihistamines. No report was noted for other antihistamines. The patients' age ranged from 6 to 71 years, with a female predominance (76.1%). Antihistamine use ranged from months to years, with pruritus developing between 1 to 5 days after discontinuation. Among the common treatment strategies adopted, cetirizine or levocetirizine re-initiation was the most effective (&lt;i&gt;n&lt;/i&gt; = 136 of 137, 99.2%), while antihistamine tapering had the lowest rate of symptoms resolution (&lt;i&gt;n&lt;/i&gt; = 11 of 33, 33.3%).&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Rebound pruritus following discontinuation of chronic cetirizine or levocetirizine use represents a clinically relevant adverse effect that warrants careful monitoring and management. Future research is required to identify the optimal treatment strategy and if the discontinuation of other antihistamines could also lead to rebound pruritus.&lt;/p&gt;</content:encoded>
         <dc:creator>
Jun Jie Benjamin Seng, 
Prawira Oka, 
Ngiap Chuan Tan
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Rebound Pruritus and Urticaria After Discontinuation of Chronic Antihistamine Use—A Scoping Review</dc:title>
         <dc:identifier>10.1111/cea.70291</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70291</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70291?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70294?af=R</link>
         <pubDate>Fri, 27 Mar 2026 20:30:22 -0700</pubDate>
         <dc:date>2026-03-27T08:30:22-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70294</guid>
         <title>Tezepelumab Reduces Alarmin Cytokine Levels in Upper Airway Epithelial Cells in Patients With Severe Asthma</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Hazel Marriott, 
Adil Adatia, 
Subhabrata Moitra, 
Paige Lacy
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Tezepelumab Reduces Alarmin Cytokine Levels in Upper Airway Epithelial Cells in Patients With Severe Asthma</dc:title>
         <dc:identifier>10.1111/cea.70294</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70294</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70294?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70275?af=R</link>
         <pubDate>Wed, 25 Mar 2026 19:34:28 -0700</pubDate>
         <dc:date>2026-03-25T07:34:28-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70275</guid>
         <title>Sputum TGF‐β Level Is Increased in Allergic Rhinitis and Related to Small Airways Dysfunction</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Amaryllis Haccuria, 
Florence Schleich, 
Myrna Virreira‐Bermudez, 
Monique Henket, 
Andrei Malinovschi, 
Alain Van Muylem, 
Renaud Louis, 
Alain Michils
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Sputum TGF‐β Level Is Increased in Allergic Rhinitis and Related to Small Airways Dysfunction</dc:title>
         <dc:identifier>10.1111/cea.70275</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70275</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70275?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70290?af=R</link>
         <pubDate>Wed, 25 Mar 2026 16:44:08 -0700</pubDate>
         <dc:date>2026-03-25T04:44:08-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70290</guid>
         <title>Allergy in Australia</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Robert J. Boyle
</dc:creator>
         <category>EDITORIAL</category>
         <dc:title>Allergy in Australia</dc:title>
         <dc:identifier>10.1111/cea.70290</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70290</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70290?af=R</prism:url>
         <prism:section>EDITORIAL</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70240?af=R</link>
         <pubDate>Wed, 25 Mar 2026 05:00:55 -0700</pubDate>
         <dc:date>2026-03-25T05:00:55-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70240</guid>
         <title>Perinatal Exposures Are Related to Atopic Symptom Development in Early Childhood</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Gina J. van Beveren, 
Nynke L. Harschel, 
Erik Tieken, 
Sjoerd M. Euser, 
Frans B. Plötz, 
Wouter J. de Waal, 
Ivo van der Lee, 
Suzanne W. J. Terheggen‐Lagro, 
Marlies A. van Houten, 
Debby Bogaert
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Perinatal Exposures Are Related to Atopic Symptom Development in Early Childhood</dc:title>
         <dc:identifier>10.1111/cea.70240</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70240</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70240?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70289?af=R</link>
         <pubDate>Tue, 24 Mar 2026 17:43:47 -0700</pubDate>
         <dc:date>2026-03-24T05:43:47-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70289</guid>
         <title>Mechanism of Cardiac Arrest in Fatal Anaphylaxis</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
This population‐based retrospective cohort study of clinical deterioration in anaphylaxis deaths identifies bronchospasm as the preponderant cause of cardiac arrest, especially in food and drug allergen exposures. The clinical implication is that anaphylaxis guidelines require appropriate emphasis on respiratory involvement and treatment to prevent deaths.

ABSTRACT

Introduction
Anaphylaxis is a short duration, potentially catastrophic allergic reaction where a rapid return to a person's baseline can be expected if vital organ function can be supported. Fatal anaphylaxis is a rare but potentially preventable cause of death at all ages. The three main mechanisms of rapid organ system failure leading to cardiac arrest in anaphylaxis are upper airway obstruction, lower respiratory obstruction principally from bronchospasm and cardiovascular failure. We aimed to measure the frequency and timing of each organ failure type leading to fatal anaphylaxis to further inform treatment recommendations.


Methods
We performed a population‐based retrospective cohort analysis for the period 1 January 2003 to 31 December 2022 using Australian clinical data contained within the National Coronial Information System. The primary outcome was the primary organ that failed leading to initial physiological decompensation. Secondary objectives were to compare the time course of deterioration and complications between allergen groups. Multivariate logistic regression was used to quantify adjusted odds ratios between allergen categories for each of the three organ failure types.


Results
There were 371 anaphylaxis deaths for the study period (mean age 55.7 years, male 58.5%) with the primary outcome recorded in 250 (67.4%). In overall all‐cause anaphylaxis fatalities, the most common organ failure was bronchospasm‐induced respiratory failure (n = 153, 61.2%). Cardiovascular failure was less common (n = 73, 29.2%) and upper airway obstruction occurred in 24 (9.6%). There were significant differences in the primary organ system failure according to allergen trigger categories. Fatal food anaphylaxis was exclusively associated with respiratory failure (bronchospasm 94.8%, upper airway 5.2%).


Conclusion
We found that respiratory failure rather than cardiovascular failure was the most common cause of cardiorespiratory arrest in fatal anaphylaxis. Death from food‐triggered anaphylaxis appears to be exclusively a primary respiratory event. International anaphylaxis guidelines require appropriate emphasis on respiratory symptoms and treatment to further reduce the risk of anaphylaxis fatalities.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/9c011826-edde-4cf9-88b3-064772143683/cea70289-toc-0001-m.png"
     alt="Mechanism of Cardiac Arrest in Fatal Anaphylaxis"/&gt;
&lt;p&gt;This population-based retrospective cohort study of clinical deterioration in anaphylaxis deaths identifies bronchospasm as the preponderant cause of cardiac arrest, especially in food and drug allergen exposures. The clinical implication is that anaphylaxis guidelines require appropriate emphasis on respiratory involvement and treatment to prevent deaths.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Anaphylaxis is a short duration, potentially catastrophic allergic reaction where a rapid return to a person's baseline can be expected if vital organ function can be supported. Fatal anaphylaxis is a rare but potentially preventable cause of death at all ages. The three main mechanisms of rapid organ system failure leading to cardiac arrest in anaphylaxis are upper airway obstruction, lower respiratory obstruction principally from bronchospasm and cardiovascular failure. We aimed to measure the frequency and timing of each organ failure type leading to fatal anaphylaxis to further inform treatment recommendations.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;We performed a population-based retrospective cohort analysis for the period 1 January 2003 to 31 December 2022 using Australian clinical data contained within the National Coronial Information System. The primary outcome was the primary organ that failed leading to initial physiological decompensation. Secondary objectives were to compare the time course of deterioration and complications between allergen groups. Multivariate logistic regression was used to quantify adjusted odds ratios between allergen categories for each of the three organ failure types.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;There were 371 anaphylaxis deaths for the study period (mean age 55.7 years, male 58.5%) with the primary outcome recorded in 250 (67.4%). In overall all-cause anaphylaxis fatalities, the most common organ failure was bronchospasm-induced respiratory failure (&lt;i&gt;n&lt;/i&gt; = 153, 61.2%). Cardiovascular failure was less common (&lt;i&gt;n&lt;/i&gt; = 73, 29.2%) and upper airway obstruction occurred in 24 (9.6%). There were significant differences in the primary organ system failure according to allergen trigger categories. Fatal food anaphylaxis was exclusively associated with respiratory failure (bronchospasm 94.8%, upper airway 5.2%).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;We found that respiratory failure rather than cardiovascular failure was the most common cause of cardiorespiratory arrest in fatal anaphylaxis. Death from food-triggered anaphylaxis appears to be exclusively a primary respiratory event. International anaphylaxis guidelines require appropriate emphasis on respiratory symptoms and treatment to further reduce the risk of anaphylaxis fatalities.&lt;/p&gt;</content:encoded>
         <dc:creator>
Ben A. McKenzie, 
Stuart D. Marshall, 
Lena A. Sanci, 
Catriona Moynihan, 
Chris Selman, 
Jo A. Douglass
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Mechanism of Cardiac Arrest in Fatal Anaphylaxis</dc:title>
         <dc:identifier>10.1111/cea.70289</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70289</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70289?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70280?af=R</link>
         <pubDate>Sun, 22 Mar 2026 17:50:12 -0700</pubDate>
         <dc:date>2026-03-22T05:50:12-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70280</guid>
         <title>Prevalence, Incidence, and Persistence of Food Allergies Among U.S. Adults: A Longitudinal Population‐Based Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Maurice M. Ohayon, 
Stéphanie Duhoux, 
Marie‐Lise Côté
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Prevalence, Incidence, and Persistence of Food Allergies Among U.S. Adults: A Longitudinal Population‐Based Study</dc:title>
         <dc:identifier>10.1111/cea.70280</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70280</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70280?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70270?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70270</guid>
         <title>Vale Professor Shamji</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 198-199, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Robert J. Boyle, 
Robin Gore
</dc:creator>
         <category>EDITORIAL</category>
         <dc:title>Vale Professor Shamji</dc:title>
         <dc:identifier>10.1111/cea.70270</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70270</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70270?af=R</prism:url>
         <prism:section>EDITORIAL</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70221?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70221</guid>
         <title>New Perspectives on Effects of Biologics on Mannitol Airway Hyperresponsiveness</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 195-197, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Robert Greig, 
Philipp Suter, 
Rory Chan, 
Brian Lipworth
</dc:creator>
         <category>EDITORIAL</category>
         <dc:title>New Perspectives on Effects of Biologics on Mannitol Airway Hyperresponsiveness</dc:title>
         <dc:identifier>10.1111/cea.70221</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70221</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70221?af=R</prism:url>
         <prism:section>EDITORIAL</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70259?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70259</guid>
         <title>Issue Information</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 193-194, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator/>
         <category>ISSUE INFORMATION</category>
         <dc:title>Issue Information</dc:title>
         <dc:identifier>10.1111/cea.70259</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70259</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70259?af=R</prism:url>
         <prism:section>ISSUE INFORMATION</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70224?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70224</guid>
         <title>Correction to “Diagnostic Performance of Serial Serum Total Tryptase Measurement to Differentiate Positive From Negative Allergy Testing Among Patients With Suspected Perioperative Hypersensitivity”</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 306-306, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator/>
         <category>CORRECTION</category>
         <dc:title>Correction to “Diagnostic Performance of Serial Serum Total Tryptase Measurement to Differentiate Positive From Negative Allergy Testing Among Patients With Suspected Perioperative Hypersensitivity”</dc:title>
         <dc:identifier>10.1111/cea.70224</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70224</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70224?af=R</prism:url>
         <prism:section>CORRECTION</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70257?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70257</guid>
         <title>Featured Cover</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page i-i, March 2026. </description>
         <dc:description>
The cover image is based on the article Longitudinal Blood Transcriptome Analysis Reveals Dynamic Gene Expression Patterns in Patients With Allergic Rhinitis Following House Dust Mite Subcutaneous Immunotherapy by Chang Liu et al., https://doi.org/10.1111/cea.70158.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/b43c52e8-2143-4452-a878-311cd41b2a18/cea70257-toc-0001-m.png"
     alt="Featured Cover"/&gt;
&lt;p&gt;The cover image is based on the article &lt;i&gt;Longitudinal Blood Transcriptome Analysis Reveals Dynamic Gene Expression Patterns in Patients With Allergic Rhinitis Following House Dust Mite Subcutaneous Immunotherapy&lt;/i&gt; by Chang Liu et al., &lt;a target="_blank"
   title="Link to external resource"
   href="https://doi.org/10.1111/cea.70158"&gt;https://doi.org/10.1111/cea.70158&lt;/a&gt;.
&lt;/p&gt;
&lt;br/&gt;
</content:encoded>
         <dc:creator>
Chang Liu, 
Shikun He, 
Jinxiu Zhang, 
Jincai Zhu, 
Jianxia Rao, 
Kanghua Wang, 
Yunping Fan, 
Yueqi Sun
</dc:creator>
         <category>FEATURED COVER</category>
         <dc:title>Featured Cover</dc:title>
         <dc:identifier>10.1111/cea.70257</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70257</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70257?af=R</prism:url>
         <prism:section>FEATURED COVER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70153?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70153</guid>
         <title>Allergen‐Specific Human Monoclonal IgG Antibodies for Use in Passive Allergy Immunotherapy</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 200-211, March 2026. </description>
         <dc:description>
ABSTRACT
The last decades have shown the number of subjects developing allergic rhinitis (AR), allergic asthma (AA), atopic dermatitis (AD), and food allergy rose continuously worldwide. To cure these allergic diseases, allergen‐specific immunotherapy (AIT) represents the unique treatment capable of providing clinical outcomes through the induction of long‐term immunological tolerance. Despite proven efficacy, the duration of treatment, AIT‐associated side effects, and the difficulty in identifying potential responders by diagnosis lead to poor patient compliance. Clinical investigations evidenced the role of blocking IgG antibodies induced by AIT in long‐term tolerance. These observations suggested that passive allergy immunotherapy (PAIT) with low doses of allergen‐specific blocking IgG antibodies represents an elegant alternative to frequent administrations of allergen extracts. Tremendous technological progress in the discovery/production of fully human monoclonal antibodies (mAbs) with very low immunogenicity has been made in the last decades, and these therapeutic antibodies revolutionised the treatment of cancers or infectious diseases. The recent advances in the isolation of rare allergen‐specific IgE+ B cells and the generation of human antibodies in transgenic mice made possible the production of human monoclonal blocking antibodies against any allergen, sharing the same affinity with the corresponding naturally occurring IgE. This comprehensive review will describe the first promising preclinical and clinical data obtained with antibody cocktails targeting several IgE epitopes to some key single allergens. PAIT is safe and effective for the downregulation of the allergic response. Compared with conventional extract‐based AIT, the positive outcomes could require much less dosing.
</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;The last decades have shown the number of subjects developing allergic rhinitis (AR), allergic asthma (AA), atopic dermatitis (AD), and food allergy rose continuously worldwide. To cure these allergic diseases, allergen-specific immunotherapy (AIT) represents the unique treatment capable of providing clinical outcomes through the induction of long-term immunological tolerance. Despite proven efficacy, the duration of treatment, AIT-associated side effects, and the difficulty in identifying potential responders by diagnosis lead to poor patient compliance. Clinical investigations evidenced the role of blocking IgG antibodies induced by AIT in long-term tolerance. These observations suggested that passive allergy immunotherapy (PAIT) with low doses of allergen-specific blocking IgG antibodies represents an elegant alternative to frequent administrations of allergen extracts. Tremendous technological progress in the discovery/production of fully human monoclonal antibodies (mAbs) with very low immunogenicity has been made in the last decades, and these therapeutic antibodies revolutionised the treatment of cancers or infectious diseases. The recent advances in the isolation of rare allergen-specific IgE+ B cells and the generation of human antibodies in transgenic mice made possible the production of human monoclonal blocking antibodies against any allergen, sharing the same affinity with the corresponding naturally occurring IgE. This comprehensive review will describe the first promising preclinical and clinical data obtained with antibody cocktails targeting several IgE epitopes to some key single allergens. PAIT is safe and effective for the downregulation of the allergic response. Compared with conventional extract-based AIT, the positive outcomes could require much less dosing.&lt;/p&gt;</content:encoded>
         <dc:creator>
Scott A. Smith, 
Cosby A. Stone Jr., 
Alain Jacquet
</dc:creator>
         <category>REVIEW ARTICLE</category>
         <dc:title>Allergen‐Specific Human Monoclonal IgG Antibodies for Use in Passive Allergy Immunotherapy</dc:title>
         <dc:identifier>10.1111/cea.70153</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70153</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70153?af=R</prism:url>
         <prism:section>REVIEW ARTICLE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70169?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70169</guid>
         <title>Global Burden of Elderly Atopic Dermatitis (1990–2021) and Projections to 2030: A Socio‐Demographic Index Analysis</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 264-266, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ruiqian Yao, 
Lin Du, 
Haixia Zhao, 
Xiaoyan Yang, 
Erwen Kou, 
Bo Wang, 
Yuanjie Zhu
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Global Burden of Elderly Atopic Dermatitis (1990–2021) and Projections to 2030: A Socio‐Demographic Index Analysis</dc:title>
         <dc:identifier>10.1111/cea.70169</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70169</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70169?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70174?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70174</guid>
         <title>Uncovering Mite Sensitisation: Epidemiological Insights From a General Population Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 285-287, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Laura Romero‐Sánchez, 
Francisco Gude, 
Arturo González‐Quintela, 
Manuela Alonso‐Sampedro, 
Óscar Lado‐Baleato, 
Carmen Fernández‐Merino, 
Flora Miranda‐Pena, 
Carmen Vidal
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Uncovering Mite Sensitisation: Epidemiological Insights From a General Population Study</dc:title>
         <dc:identifier>10.1111/cea.70174</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70174</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70174?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70181?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70181</guid>
         <title>Drug Allergy Risk Stratification in Children With Immediate or Delayed Urticaria During Antibiotic Treatment</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 275-277, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Francesca Mori, 
Leonardo Tomei, 
Chiara Marzi, 
Giulia Liccioli, 
Simona Barni, 
Mattia Giovannini, 
Lucrezia Sarti, 
Benedetta Pessina, 
Lene Heise Garvey
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Drug Allergy Risk Stratification in Children With Immediate or Delayed Urticaria During Antibiotic Treatment</dc:title>
         <dc:identifier>10.1111/cea.70181</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70181</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70181?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70195?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70195</guid>
         <title>Baseline Epigenetics as a Biomarker of Mepolizumab Response in Severe Asthma</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 294-296, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Hongmei Zhang, 
Xin Jin, 
Hasan Arshad, 
Ramesh J. Kurukulaaratchy
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Baseline Epigenetics as a Biomarker of Mepolizumab Response in Severe Asthma</dc:title>
         <dc:identifier>10.1111/cea.70195</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70195</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70195?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70167?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70167</guid>
         <title>Managing Drug Hypersensitivities: Clinicians' Perceptions on an Optimised Documentation Tool With De‐Labelling Feature</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 281-284, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Veronique Shiwa, 
Sven Van Laere, 
Martine Grosber, 
Pieter Cornu
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Managing Drug Hypersensitivities: Clinicians' Perceptions on an Optimised Documentation Tool With De‐Labelling Feature</dc:title>
         <dc:identifier>10.1111/cea.70167</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70167</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70167?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70170?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70170</guid>
         <title>Exploring the Disease Duration of Urticaria and Associated Determinants in Primary Care</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 271-274, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
R. Soegiharto, 
B. J. Hengevelt, 
N. Boekema‐Bakker, 
I. A. M. Groenewegen, 
A. C. Knulst, 
J. M. P. A. Van den Reek, 
H. Röckmann
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Exploring the Disease Duration of Urticaria and Associated Determinants in Primary Care</dc:title>
         <dc:identifier>10.1111/cea.70170</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70170</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70170?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70178?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70178</guid>
         <title>Barriers to Seeking Mental Health Services for Atopic Dermatitis Patients and Caregivers</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 267-270, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Allison R. Loiselle, 
Courtney A. Chau, 
Jessica K. Johnson, 
Jennifer LeBovidge, 
Lynda Schneider, 
Wendy Smith Begolka
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Barriers to Seeking Mental Health Services for Atopic Dermatitis Patients and Caregivers</dc:title>
         <dc:identifier>10.1111/cea.70178</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70178</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70178?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70200?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70200</guid>
         <title>Clinical Characteristics, Treatment Patterns and Outcomes of Oral Corticosteroid–Dependent Asthma in Real‐World Practice: A Nationwide Population‐Based Study in Korea</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 300-303, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>Hyun Lee, Kyungjoo Kim, Joon Young Choi, Chin Kook Rhee, Ji‐Yong Moon, Kyung Hoon Min, Yong Il Hwang, Kwang Ha Yoo, Seong Yong Lim,  on behalf of the Korean Asthma Study Group</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Clinical Characteristics, Treatment Patterns and Outcomes of Oral Corticosteroid–Dependent Asthma in Real‐World Practice: A Nationwide Population‐Based Study in Korea</dc:title>
         <dc:identifier>10.1111/cea.70200</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70200</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70200?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70191?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70191</guid>
         <title>Clustering of the Bronchial Epithelial Immune Response to Viral Stimulation in Patients With Asthma Identifies Clinically Recognisable Epithelial Exacerbation Response Profiles</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 291-293, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Laurits Frøssing, 
Morten Hvidtfeldt, 
Juan Jose Nieto‐Fontarigo, 
Sangeeta Ramu, 
Mandy Menzel, 
Lise Lotte Eriksen, 
Nanna Dyhre‐Petersen, 
Asger Sverrild, 
Lena Uller, 
Celeste Porsbjerg
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Clustering of the Bronchial Epithelial Immune Response to Viral Stimulation in Patients With Asthma Identifies Clinically Recognisable Epithelial Exacerbation Response Profiles</dc:title>
         <dc:identifier>10.1111/cea.70191</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70191</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70191?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70197?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70197</guid>
         <title>Engineering Chimeric Hypoallergens for Safer and More Effective House Dust Mite Allergy Vaccines</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 288-290, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Eduardo S. da Silva, 
Antônio M. S. Fernandes, 
Elisânia F. Silveira, 
Raphael C. Silva, 
Leonardo F. Santiago, 
Luis F. S. Garcés, 
Sara Huber, 
Sabrina Wildner, 
Tafarel A. Souza, 
Vitor S. Alves, 
Lorena M. de Souza, 
Deise S. Vilas‐Bôas, 
Peter Briza, 
Peter Lackner, 
Luis G. C. Pacheco, 
Neuza M. Alcântara‐Neves, 
Fatima Ferreira, 
Carina S. Pinheiro
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Engineering Chimeric Hypoallergens for Safer and More Effective House Dust Mite Allergy Vaccines</dc:title>
         <dc:identifier>10.1111/cea.70197</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70197</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70197?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70199?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70199</guid>
         <title>Effectiveness and Safety of Mepolizumab in Allergic Bronchopulmonary Aspergillosis (ABPA): Real‐World Experience From a Chinese Retrospective Case Series</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 297-299, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Xu Li, 
Peize Liu, 
Tingting Gao, 
Jingjing Wang, 
Mengwei Wu, 
Haoyuan Li, 
Yinghui Qu, 
Ruichen Du, 
Liang Dong, 
Qian Qi, 
Lili Zhi
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Effectiveness and Safety of Mepolizumab in Allergic Bronchopulmonary Aspergillosis (ABPA): Real‐World Experience From a Chinese Retrospective Case Series</dc:title>
         <dc:identifier>10.1111/cea.70199</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70199</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70199?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70151?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70151</guid>
         <title>The Incidence of Addiction and Its Risk Factors in Chinese Chronic Urticaria Patients</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 278-280, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Xinyu Shui, 
Yu Jiang, 
Cong Peng, 
Qiaozhi Cao, 
Jie Li
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>The Incidence of Addiction and Its Risk Factors in Chinese Chronic Urticaria Patients</dc:title>
         <dc:identifier>10.1111/cea.70151</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70151</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70151?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70228?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70228</guid>
         <title>A Single‐Nucleotide Polymorphism as a Surrogate Marker for Hereditary Alpha‐Tryptasemia: Are We There Yet?</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 304-305, March 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Yannick Chantran
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>A Single‐Nucleotide Polymorphism as a Surrogate Marker for Hereditary Alpha‐Tryptasemia: Are We There Yet?</dc:title>
         <dc:identifier>10.1111/cea.70228</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70228</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70228?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70158?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70158</guid>
         <title>Longitudinal Blood Transcriptome Analysis Reveals Dynamic Gene Expression Patterns in Patients With Allergic Rhinitis Following House Dust Mite Subcutaneous Immunotherapy</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 252-263, March 2026. </description>
         <dc:description>
AR inhibits Th1 immune responses and induces B cell activation. SCIT dynamically modulates blood gene expression gradually normalised. SCIT enhanced type I interferon responses and antiviral pathways while decreasing B cell activation and inflammatory responses.

ABSTRACT

Introduction
Subcutaneous immunotherapy (SCIT) is a well‐established treatment for inducing immune tolerance in patients with allergic rhinitis (AR). However, the precise molecular mechanisms by which SCIT induces immune tolerance, particularly at the transcriptomic level over the treatment course, have not been fully elucidated. This study aimed to investigate the molecular mechanisms of SCIT by analysing changes in peripheral blood gene expression profiles in AR patients over time.


Methods
Whole blood samples were prospectively collected from 30 AR patients (16 paediatric, 14 adult) and 10 healthy controls. RNA sequencing was performed at baseline and at 3, 6 and 12 months of SCIT. Differentially expressed genes (DEGs) were identified, and pathway enrichment, immune cell deconvolution and weighted gene co‐expression network analysis were conducted to explore immune regulation and tolerance mechanisms.


Results
AR patients showed 1180 DEGs compared to healthy controls, with upregulated genes related to B‐cell activation and downregulated genes linked to Th1 differentiation. Both paediatric and adult cohorts exhibited consistent transcriptomic changes, characterised by progressive normalisation of gene expression, with the number of DEGs decreasing over time and significant convergence towards healthy control profiles by 12 months. SCIT enhanced type I interferon responses and antiviral pathways while reducing B‐cell activation and inflammatory responses. Immune cell analysis revealed increased regulatory T cells and dendritic cells by 6 months and reduced Th2 cells and eosinophils by 12 months. Key immune‐related hub genes, including CD19, CD79A, CD79B, CD22, IFIH1, STAT1, DHX58, TLR4, IL1B and TLR1, were identified as central to SCIT efficacy.


Conclusion
SCIT dynamically modulates blood gene expression profiles in AR patients, inducing immune tolerance and reducing inflammatory responses. These findings enhance understanding of the molecular mechanisms of SCIT and highlight potential biomarkers for predicting and monitoring treatment efficacy.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/359d7d9b-c006-4a3b-93bd-cab2ec4c8300/cea70158-toc-0001-m.png"
     alt="Longitudinal Blood Transcriptome Analysis Reveals Dynamic Gene Expression Patterns in Patients With Allergic Rhinitis Following House Dust Mite Subcutaneous Immunotherapy"/&gt;
&lt;p&gt;AR inhibits Th1 immune responses and induces B cell activation. SCIT dynamically modulates blood gene expression gradually normalised. SCIT enhanced type I interferon responses and antiviral pathways while decreasing B cell activation and inflammatory responses.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Subcutaneous immunotherapy (SCIT) is a well-established treatment for inducing immune tolerance in patients with allergic rhinitis (AR). However, the precise molecular mechanisms by which SCIT induces immune tolerance, particularly at the transcriptomic level over the treatment course, have not been fully elucidated. This study aimed to investigate the molecular mechanisms of SCIT by analysing changes in peripheral blood gene expression profiles in AR patients over time.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Whole blood samples were prospectively collected from 30 AR patients (16 paediatric, 14 adult) and 10 healthy controls. RNA sequencing was performed at baseline and at 3, 6 and 12 months of SCIT. Differentially expressed genes (DEGs) were identified, and pathway enrichment, immune cell deconvolution and weighted gene co-expression network analysis were conducted to explore immune regulation and tolerance mechanisms.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;AR patients showed 1180 DEGs compared to healthy controls, with upregulated genes related to B-cell activation and downregulated genes linked to Th1 differentiation. Both paediatric and adult cohorts exhibited consistent transcriptomic changes, characterised by progressive normalisation of gene expression, with the number of DEGs decreasing over time and significant convergence towards healthy control profiles by 12 months. SCIT enhanced type I interferon responses and antiviral pathways while reducing B-cell activation and inflammatory responses. Immune cell analysis revealed increased regulatory T cells and dendritic cells by 6 months and reduced Th2 cells and eosinophils by 12 months. Key immune-related hub genes, including &lt;i&gt;CD19, CD79A, CD79B, CD22, IFIH1, STAT1, DHX58, TLR4, IL1B&lt;/i&gt; and &lt;i&gt;TLR1,&lt;/i&gt; were identified as central to SCIT efficacy.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;SCIT dynamically modulates blood gene expression profiles in AR patients, inducing immune tolerance and reducing inflammatory responses. These findings enhance understanding of the molecular mechanisms of SCIT and highlight potential biomarkers for predicting and monitoring treatment efficacy.&lt;/p&gt;</content:encoded>
         <dc:creator>
Chang Liu, 
Shikun He, 
Jinxiu Zhang, 
Jincai Zhu, 
Jianxia Rao, 
Kanghua Wang, 
Yunping Fan, 
Yueqi Sun
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Longitudinal Blood Transcriptome Analysis Reveals Dynamic Gene Expression Patterns in Patients With Allergic Rhinitis Following House Dust Mite Subcutaneous Immunotherapy</dc:title>
         <dc:identifier>10.1111/cea.70158</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70158</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70158?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70184?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70184</guid>
         <title>Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N‐ERD Patients</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 227-242, March 2026. </description>
         <dc:description>
Dupilumab therapy reduced elevated type 2 cytokine responses post‐ASA provocation in N‐ERD patients, independent of ASA tolerance, and revealed novel mechanistic insights by modulating acute type 2 immunity. Transcriptomic analysis showed concurrent downregulation of lipid and peroxisome pathways during ASA challenge in N‐ERD patients after 24 weeks of dupilumab. ASA, acetylsalicylic acid; CRSwNP, chronic rhinosinusitis with nasal polyps; N‐ERD, Non‐steroidal anti‐inflammatory drug (NSAID)‐exacerbated respiratory disease.

ABSTRACT

Background
Non‐steroidal anti‐inflammatory drug‐exacerbated respiratory disease (N‐ERD) is characterised by the clinical triad of hypersensitivity to NSAIDs, nasal polyposis, and asthma. The cells and mediators causing acute symptoms when driving the hypersensitivity reaction to acetylsalicylic acid (ASA) ingestion, remain poorly defined.


Objective
To investigate the dynamics of nasal mediators during ASA provocation in N‐ERD patients before and 24 weeks after therapy with the IL‐4 receptor alpha‐blocking antibody dupilumab (EudraCT (2019‐004889‐18) and ClinicalTrials.gov (NCT04442256)).


Methods
Nasal mucosal lining fluids of patients with N‐ERD, chronic rhinosinusitis patients with nasal polyp (CRSwNP) and healthy disease controls were collected at selected time points up to 2 h after ASA provocation. Analysis of thirty‐three different inflammatory mediators as well as transcriptomic profiling was performed. In N‐ERD patients, provocation was repeated after 24 weeks of dupilumab therapy.


Results
Sixty minutes after provocation with ASA, N‐ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL‐5 and eotaxin‐3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., AREG) as well as enhanced downregulation of lipid (i.e., ALOX15) and peroxisome metabolisms (i.e., NOS2) at ASA provocation after dupilumab therapy.


Conclusion and Clinical Relevance
Treatment with dupilumab leads to reduced nasal type 2 cytokine secretion and distinct changes in transcriptomic profile during ASA provocation, but changes in type 2 mediators show no association with tolerance development.


Trial Registration
EudraCT (2019‐004889‐18) and ClinicalTrials.gov (NCT04442256)

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/807fface-5264-4450-8b24-f69720e93ee8/cea70184-toc-0001-m.png"
     alt="Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N-ERD Patients"/&gt;
&lt;p&gt;Dupilumab therapy reduced elevated type 2 cytokine responses post-ASA provocation in N-ERD patients, independent of ASA tolerance, and revealed novel mechanistic insights by modulating acute type 2 immunity. Transcriptomic analysis showed concurrent downregulation of lipid and peroxisome pathways during ASA challenge in N-ERD patients after 24 weeks of dupilumab. ASA, acetylsalicylic acid; CRSwNP, chronic rhinosinusitis with nasal polyps; N-ERD, Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Non-steroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) is characterised by the clinical triad of hypersensitivity to NSAIDs, nasal polyposis, and asthma. The cells and mediators causing acute symptoms when driving the hypersensitivity reaction to acetylsalicylic acid (ASA) ingestion, remain poorly defined.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To investigate the dynamics of nasal mediators during ASA provocation in N-ERD patients before and 24 weeks after therapy with the IL-4 receptor alpha-blocking antibody dupilumab (EudraCT (2019-004889-18) and &lt;a target="_blank"
   title="Link to external resource"
   href="http://clinicaltrials.gov"&gt;ClinicalTrials.gov&lt;/a&gt; (NCT04442256)).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Nasal mucosal lining fluids of patients with N-ERD, chronic rhinosinusitis patients with nasal polyp (CRSwNP) and healthy disease controls were collected at selected time points up to 2 h after ASA provocation. Analysis of thirty-three different inflammatory mediators as well as transcriptomic profiling was performed. In N-ERD patients, provocation was repeated after 24 weeks of dupilumab therapy.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Sixty minutes after provocation with ASA, N-ERD patients showed a significant increase in type 2 associated cytokines (i.e., TSLP, IL-5 and eotaxin-3) as compared to the other patient groups. This effect was diminished after 24 weeks of dupilumab therapy and was independent of the development of ASA tolerance. Transcriptomics revealed dampened upregulation of type 2 associated pathway genes (i.e., &lt;i&gt;AREG&lt;/i&gt;) as well as enhanced downregulation of lipid (i.e., &lt;i&gt;ALOX15&lt;/i&gt;) and peroxisome metabolisms (i.e., &lt;i&gt;NOS2&lt;/i&gt;) at ASA provocation after dupilumab therapy.&lt;/p&gt;
&lt;h2&gt;Conclusion and Clinical Relevance&lt;/h2&gt;
&lt;p&gt;Treatment with dupilumab leads to reduced nasal type 2 cytokine secretion and distinct changes in transcriptomic profile during ASA provocation, but changes in type 2 mediators show no association with tolerance development.&lt;/p&gt;
&lt;h2&gt;Trial Registration&lt;/h2&gt;
&lt;p&gt;EudraCT (2019-004889-18) and &lt;a target="_blank"
   title="Link to external resource"
   href="http://clinicaltrials.gov"&gt;ClinicalTrials.gov&lt;/a&gt; (NCT04442256)&lt;/p&gt;</content:encoded>
         <dc:creator>
Julia Eckl‐Dorna, 
Christina Morgenstern, 
Katharina Poglitsch, 
Tamara Arnoldner, 
Katharina Gangl, 
Tina J. Bartosik, 
Nicholas J. Campion, 
Aldine Tu, 
Victoria Stanek, 
Sven Schneider, 
Christine Bangert
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N‐ERD Patients</dc:title>
         <dc:identifier>10.1111/cea.70184</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70184</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70184?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70122?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70122</guid>
         <title>Towards an Optimal Decision Threshold for Specific IgE to rCan s 3 the Non‐Specific Lipid Transfer Protein of Cannabis sativa</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 243-251, March 2026. </description>
         <dc:description>
ABSTRACT

Background
Cannabis allergy is increasingly reported, with Can s 3 as a major allergen. Investigations into sensitisation to Can s 3 utilise sophisticated techniques, including the cytometric bead assay and the basophil activation test. This study aims to utilise a fluorescence enzyme immunoassay to quantify sIgE to Can s 3, employing a recombinant Can s 3 protein.


Methods
This study included 104 cannabis allergic patients, 20 healthy controls and 70 exposed atopic controls. Specific IgE by a fluorescence enzyme immunoassay or cytometric bead assay and the basophil activation test all used the same recombinant allergen. Two‐graph ROC curves were used to determine the clinically validated allergen‐specific cut‐off for maximal sensitivity and specificity and to facilitate direct comparison of the test performances.


Results
Twenty‐two individuals were non‐responding in the basophil activation test and were excluded from all analyses involving basophil activation test results. The clinically validated cut‐off points are &gt; 0.16 kUA/L, ≥ 0.14 kUA/L and &gt; 5% for a fluorescence enzyme immunoassay, cytometric bead assay and basophil activation test, respectively. Utilising these thresholds, the fluorescence enzyme immunoassay exhibited a sensitivity of 72% and specificity of 74%, the cytometric bead assay demonstrated a sensitivity of 49% and specificity of 89%. In responders, the basophil activation test exhibited a sensitivity of 51% and specificity of 82%. Remarkably, low positive fluorescence enzyme immunoassay results, particularly below 0.35 kUA/L, are negative for both cytometric bead assay and basophil activation test. Conversely, utilising the conventional threshold of &gt; 0.35 kUA/L, the sIgE a fluorescence enzyme immunoassay results exhibited greater congruence with those of the cytometric bead assay and basophil activation test.


Conclusion
This study underscores the complexity of establishing an optimal decision threshold for the sIgE rCan s 3 fluorescence enzyme immunoassay and indicates that the clinically validated decision cut‐off may not always represent the most efficacious approach.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Cannabis allergy is increasingly reported, with Can s 3 as a major allergen. Investigations into sensitisation to Can s 3 utilise sophisticated techniques, including the cytometric bead assay and the basophil activation test. This study aims to utilise a fluorescence enzyme immunoassay to quantify sIgE to Can s 3, employing a recombinant Can s 3 protein.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;This study included 104 cannabis allergic patients, 20 healthy controls and 70 exposed atopic controls. Specific IgE by a fluorescence enzyme immunoassay or cytometric bead assay and the basophil activation test all used the same recombinant allergen. Two-graph ROC curves were used to determine the clinically validated allergen-specific cut-off for maximal sensitivity and specificity and to facilitate direct comparison of the test performances.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Twenty-two individuals were non-responding in the basophil activation test and were excluded from all analyses involving basophil activation test results. The clinically validated cut-off points are &lt;span style="text-decoration:underline"&gt;&amp;gt;&lt;/span&gt; 0.16 kU&lt;sub&gt;A&lt;/sub&gt;/L, ≥ 0.14 kU&lt;sub&gt;A&lt;/sub&gt;/L and &amp;gt; 5% for a fluorescence enzyme immunoassay, cytometric bead assay and basophil activation test, respectively. Utilising these thresholds, the fluorescence enzyme immunoassay exhibited a sensitivity of 72% and specificity of 74%, the cytometric bead assay demonstrated a sensitivity of 49% and specificity of 89%. In responders, the basophil activation test exhibited a sensitivity of 51% and specificity of 82%. Remarkably, low positive fluorescence enzyme immunoassay results, particularly below 0.35 kU&lt;sub&gt;A&lt;/sub&gt;/L, are negative for both cytometric bead assay and basophil activation test. Conversely, utilising the conventional threshold of &lt;span style="text-decoration:underline"&gt;&amp;gt;&lt;/span&gt; 0.35 kU&lt;sub&gt;A&lt;/sub&gt;/L, the sIgE a fluorescence enzyme immunoassay results exhibited greater congruence with those of the cytometric bead assay and basophil activation test.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study underscores the complexity of establishing an optimal decision threshold for the sIgE rCan s 3 fluorescence enzyme immunoassay and indicates that the clinically validated decision cut-off may not always represent the most efficacious approach.&lt;/p&gt;</content:encoded>
         <dc:creator>
Didier G. Ebo, 
Christel Mertens, 
Michel Van Houdt, 
Margo Hagendorens, 
Hans‐Peter Rihs, 
Alessandro Toscano, 
Michiel Beyens, 
Vito Sabato, 
Athina L. Van Gasse, 
Jessy Elst
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Towards an Optimal Decision Threshold for Specific IgE to rCan s 3 the Non‐Specific Lipid Transfer Protein of Cannabis sativa</dc:title>
         <dc:identifier>10.1111/cea.70122</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70122</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70122?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70162?af=R</link>
         <pubDate>Sun, 22 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-22T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDate>
         <prism:coverDisplayDate>Sun, 01 Mar 2026 00:00:00 -0800</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/cea.70162</guid>
         <title>Early and Sustained Asthma Control and Remission in Real‐World Patients With Severe Eosinophilic Asthma Treated With Benralizumab: XALOC‐2</title>
         <description>Clinical &amp;amp;Experimental Allergy, Volume 56, Issue 3, Page 212-226, March 2026. </description>
         <dc:description>
Real‐world patients with severe eosinophilic asthma treated with benralizumab showed early and sustained improvements in symptoms. Clinically meaningful improvements began as early as one week after benralizumab initiation, regardless of previous biologic use, and further improved over the following year. The 3‐component clinical remission criteria were met in more than a quarter of patients at Week 56.

ABSTRACT

Background
Prospective real‐world data concerning the early and sustained effects of benralizumab on asthma control in patients with severe eosinophilic asthma (SEA) is lacking.


Methods
XALOC‐2 is a prospective, observational, multi‐national, real‐world study in adults with SEA treated with benralizumab. This integrated analysis assessed Asthma Control Questionnaire (ACQ) scores, achievement of 3‐component clinical remission (which included well‐controlled symptoms [ACQ score ≤ 0.75], no exacerbations, and no use of maintenance oral corticosteroids [mOCS]), and other clinical outcomes, over a 12‐month baseline period and up to Week 56. Associations between remission status and key baseline characteristics were also assessed.


Results
535 patients were included. Median (interquartile range) ACQ score at baseline was 3.0 (2.2–3.8). At Week 1, 58.0% (282/486) of patients had ACQ score reductions of ≥ 0.5 points (minimal clinically important difference [MCID]) and 35.0% (170/486) had reductions of ≥ 1 point (2× MCID). By Week 56, these increased to 78.6% (276/351) and 62.1% (218/351), respectively. Improved asthma control after benralizumab initiation was similar irrespective of previous biologic use status. By Week 56, clinical remission criteria were achieved in 26.7% (70/262) of patients versus 0% (0/374) at baseline. No mOCS use, lower body mass index, better asthma symptom control and higher peak blood eosinophil count at baseline were associated with meeting 3‐component clinical remission criteria at Week 56.


Conclusions
Real‐world patients receiving benralizumab showed early and sustained improvements in asthma symptoms, regardless of previous biologic use. More than a quarter of patients achieved clinical asthma remission after 1 year of benralizumab treatment.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/6147f46a-484e-4afd-b774-be809d3cbaca/cea70162-toc-0001-m.png"
     alt="Early and Sustained Asthma Control and Remission in Real-World Patients With Severe Eosinophilic Asthma Treated With Benralizumab: XALOC-2"/&gt;
&lt;p&gt;Real-world patients with severe eosinophilic asthma treated with benralizumab showed early and sustained improvements in symptoms. Clinically meaningful improvements began as early as one week after benralizumab initiation, regardless of previous biologic use, and further improved over the following year. The 3-component clinical remission criteria were met in more than a quarter of patients at Week 56.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Prospective real-world data concerning the early and sustained effects of benralizumab on asthma control in patients with severe eosinophilic asthma (SEA) is lacking.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;XALOC-2 is a prospective, observational, multi-national, real-world study in adults with SEA treated with benralizumab. This integrated analysis assessed Asthma Control Questionnaire (ACQ) scores, achievement of 3-component clinical remission (which included well-controlled symptoms [ACQ score ≤ 0.75], no exacerbations, and no use of maintenance oral corticosteroids [mOCS]), and other clinical outcomes, over a 12-month baseline period and up to Week 56. Associations between remission status and key baseline characteristics were also assessed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;535 patients were included. Median (interquartile range) ACQ score at baseline was 3.0 (2.2–3.8). At Week 1, 58.0% (282/486) of patients had ACQ score reductions of ≥ 0.5 points (minimal clinically important difference [MCID]) and 35.0% (170/486) had reductions of ≥ 1 point (2× MCID). By Week 56, these increased to 78.6% (276/351) and 62.1% (218/351), respectively. Improved asthma control after benralizumab initiation was similar irrespective of previous biologic use status. By Week 56, clinical remission criteria were achieved in 26.7% (70/262) of patients versus 0% (0/374) at baseline. No mOCS use, lower body mass index, better asthma symptom control and higher peak blood eosinophil count at baseline were associated with meeting 3-component clinical remission criteria at Week 56.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Real-world patients receiving benralizumab showed early and sustained improvements in asthma symptoms, regardless of previous biologic use. More than a quarter of patients achieved clinical asthma remission after 1 year of benralizumab treatment.&lt;/p&gt;</content:encoded>
         <dc:creator>
Erika Penz, 
Thomas Rothe, 
Lieven Dupont, 
Trung N. Tran, 
Andrew Menzies‐Gow, 
Anat Shavit, 
David Cohen, 
Tanja Plate, 
Sheena Kayaniyil, 
An Herreman, 
Claudio Schuoler, 
Benjamin Emmanuel, 
Marek Lommatzsch
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Early and Sustained Asthma Control and Remission in Real‐World Patients With Severe Eosinophilic Asthma Treated With Benralizumab: XALOC‐2</dc:title>
         <dc:identifier>10.1111/cea.70162</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70162</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70162?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>56</prism:volume>
         <prism:number>3</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70286?af=R</link>
         <pubDate>Fri, 20 Mar 2026 00:30:52 -0700</pubDate>
         <dc:date>2026-03-20T12:30:52-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70286</guid>
         <title>Common Causative Drugs of Paediatric Drug‐Induced Dermatitis: A Population‐Based Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Hyeyone Hwang, 
Jiung Jeong, 
Soo Min Jeon, 
Jin‐Won Kwon, 
Juhee Ryu
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Common Causative Drugs of Paediatric Drug‐Induced Dermatitis: A Population‐Based Study</dc:title>
         <dc:identifier>10.1111/cea.70286</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70286</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70286?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70287?af=R</link>
         <pubDate>Thu, 19 Mar 2026 01:59:35 -0700</pubDate>
         <dc:date>2026-03-19T01:59:35-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70287</guid>
         <title>Increased TRPV6 Potentiates Interleukin‐13 Signalling in Epithelial Cells in Eosinophilic Chronic Rhinosinusitis With Nasal Polyps</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Fuying Cheng, 
Juan Liu, 
Chen Zhang, 
Qianqian Zhang, 
Jiani Chen, 
Yizhang Wang, 
Shirui Xue, 
Yufei Yang, 
Kai Xue, 
Huan Wang, 
Xicai Sun, 
Li Hu
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Increased TRPV6 Potentiates Interleukin‐13 Signalling in Epithelial Cells in Eosinophilic Chronic Rhinosinusitis With Nasal Polyps</dc:title>
         <dc:identifier>10.1111/cea.70287</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70287</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70287?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70284?af=R</link>
         <pubDate>Thu, 19 Mar 2026 01:53:03 -0700</pubDate>
         <dc:date>2026-03-19T01:53:03-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70284</guid>
         <title>Unearthing Hereditary Angioedema in India—Epidemiology From Chandigarh and Reasi, India</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ankur K. Jindal, 
Prabal Barman, 
Suprit Basu, 
Reva Tyagi, 
Archan Sil, 
Ridhima Aggarwal, 
Sanghamitra Macchua, 
Gopika Kalsotra, 
Pramod Kalsotra, 
Sendhil M. Kumaran, 
Thomas Buttgereit, 
Markus Magerl, 
Sunil Dogra
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Unearthing Hereditary Angioedema in India—Epidemiology From Chandigarh and Reasi, India</dc:title>
         <dc:identifier>10.1111/cea.70284</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70284</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70284?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70285?af=R</link>
         <pubDate>Tue, 17 Mar 2026 20:04:06 -0700</pubDate>
         <dc:date>2026-03-17T08:04:06-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70285</guid>
         <title>India's Allergy Renaissance: A Blueprint for Global Capacity Building</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Neeraj Gupta
</dc:creator>
         <category>EDITORIAL</category>
         <dc:title>India's Allergy Renaissance: A Blueprint for Global Capacity Building</dc:title>
         <dc:identifier>10.1111/cea.70285</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70285</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70285?af=R</prism:url>
         <prism:section>EDITORIAL</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70281?af=R</link>
         <pubDate>Sun, 15 Mar 2026 11:00:00 -0700</pubDate>
         <dc:date>2026-03-15T11:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70281</guid>
         <title>Development of an Enzyme Immunoassay for Detecting Urinary Tetranor‐PGDM in Patients With Food Allergy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Takeru Ishii, 
Nanae Nagata, 
Sakura Masuko, 
Rikako Inoue, 
Masaki Fujishiro, 
Tatsuro Nakamura, 
Kosuke Aritake, 
Shinya Ogawa, 
Hisako Ogasawara, 
Mami Shimada, 
Yusuke Inuzuka, 
Kotaro Umezawa, 
Sayaka Hamaguchi, 
Tatsuki Fukuie, 
Yukihiro Ohya, 
Kiwako Yamamoto‐Hanada, 
Takahisa Murata
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Development of an Enzyme Immunoassay for Detecting Urinary Tetranor‐PGDM in Patients With Food Allergy</dc:title>
         <dc:identifier>10.1111/cea.70281</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70281</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70281?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70282?af=R</link>
         <pubDate>Fri, 13 Mar 2026 04:26:03 -0700</pubDate>
         <dc:date>2026-03-13T04:26:03-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70282</guid>
         <title>Healthy Diet Intervention for Treating Atopic Dermatitis: A Pilot Randomised Controlled Trial</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Jun Jie Lim, 
Hafizah Yusri, 
Dimeng Yang, 
Jung Eun Kim, 
Mei Hui Liu, 
Fook Tim Chew
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Healthy Diet Intervention for Treating Atopic Dermatitis: A Pilot Randomised Controlled Trial</dc:title>
         <dc:identifier>10.1111/cea.70282</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70282</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70282?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70283?af=R</link>
         <pubDate>Fri, 13 Mar 2026 04:23:37 -0700</pubDate>
         <dc:date>2026-03-13T04:23:37-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70283</guid>
         <title>Asthma in Young Adults at High Risk for Allergies Is Traced Back to Immune and Microbiota Signatures in Early Childhood</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ymke A. de Jong, 
Isabella Badolati, 
Ulrika Hellberg, 
Katarína Bankóová, 
Caroline Nilsson, 
Eva Sverremark‐Ekström
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Asthma in Young Adults at High Risk for Allergies Is Traced Back to Immune and Microbiota Signatures in Early Childhood</dc:title>
         <dc:identifier>10.1111/cea.70283</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70283</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70283?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70277?af=R</link>
         <pubDate>Thu, 12 Mar 2026 00:57:51 -0700</pubDate>
         <dc:date>2026-03-12T12:57:51-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70277</guid>
         <title>ELYFANT Study Protocol: An Observational Study to Assess Awareness of and Adherence to Advice on Early Introduction of Food Allergens and Whether It Is Preventing Food Allergy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Raquel Granell, 
Mary Feeney, 
Thisanayagam Umasunthar, 
Rachel L. Peters, 
Jennifer Koplin, 
Matthew J. Ridd
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>ELYFANT Study Protocol: An Observational Study to Assess Awareness of and Adherence to Advice on Early Introduction of Food Allergens and Whether It Is Preventing Food Allergy</dc:title>
         <dc:identifier>10.1111/cea.70277</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70277</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70277?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70279?af=R</link>
         <pubDate>Tue, 10 Mar 2026 22:25:12 -0700</pubDate>
         <dc:date>2026-03-10T10:25:12-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70279</guid>
         <title>Are Phenotypic Baseline Characteristics Related to Abolition of AHR After Benralizumab and Dupilumab?</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Philipp Suter, 
Robert Greig, 
Rory Chan, 
Brian J. Lipworth
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Are Phenotypic Baseline Characteristics Related to Abolition of AHR After Benralizumab and Dupilumab?</dc:title>
         <dc:identifier>10.1111/cea.70279</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70279</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70279?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70278?af=R</link>
         <pubDate>Tue, 10 Mar 2026 09:39:49 -0700</pubDate>
         <dc:date>2026-03-10T09:39:49-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70278</guid>
         <title>Depot Extracts for Venom Immunotherapy: A Delphi Consensus on Safety and Efficacy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>Valerio Pravettoni, Matteo Martini, Donatella Bignardi, Alessandro Buonomo, Marcello Cilia, Domenico Gargano, Marina Mauro, Francesco Murzilli, Luisa Ricciardi, M. Beatrice Bilò,  on behalf of the Allergy Venom Expert group, Patrizia Bonadonna, Elisa Boni, Linda Borgonovo, Maria Chiara Braschi, Federica Corradi, Antonello Desanctis, M. Pia Dolcher, Francesca Emiliani, Giovanni Florio, Francesco Marchi, Fulvia Marengo, Irene Martignago, M. Carmela Montera, Eustachio Nettis, Donatella Preziosi, Federica Rivolta</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Depot Extracts for Venom Immunotherapy: A Delphi Consensus on Safety and Efficacy</dc:title>
         <dc:identifier>10.1111/cea.70278</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70278</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70278?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70276?af=R</link>
         <pubDate>Tue, 10 Mar 2026 09:25:34 -0700</pubDate>
         <dc:date>2026-03-10T09:25:34-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70276</guid>
         <title>Patient‐Derived IgG Epitope Mapping of Bet v 1 Reveals Hypoallergenic Peptide Candidates for Safe and Next‐Generation Allergen Immunotherapy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Mapping IgG epitopes of the major birch allergen Bet v 1 identified patient‐derived, hypoallergenic peptides that did not trigger degranulation. These findings support a novel, safer approach for peptide‐based allergen immunotherapy that leverages naturally induced IgG specificities from allergic individuals.

ABSTRACT

Background
Allergen immunotherapy (AIT) is the only curative treatment for allergic diseases, primarily by inducing allergen‐neutralising IgG antibodies. However, its use is limited by frequent allergic adverse events.


Objective
To facilitate the design of IgG‐epitope‐based peptide vaccines, this study aimed to identify IgG‐binding regions on the major birch pollen allergen, Bet v 1, using patient‐derived immune profiles.


Methods
Blood samples were collected from 30 birch pollen‐allergic patients, both AIT‐treated and untreated; healthy individuals were included as controls. Sera were analysed for allergen‐specific IgE, IgG, and IgG4, and basophil degranulation inhibition was assessed in humanised RBL cells and blood from allergic individuals. We used DropMap microfluidics for single‐cell affinity profiling of IgG‐ and IgG4‐secreting B cells. IgG epitopes were mapped using overlapping peptides and CLIPS technology. Candidate AIT peptides were synthesised on solid phase via Fmoc strategy, and their allergenicity was assessed in basophil degranulation and cellular antigen stimulation assays.


Results
Sera from AIT‐treated patients exhibited elevated IgG and IgG4 levels and enhanced inhibition of basophil degranulation. Single‐cell analysis indicated IgG‐affinity maturation with AIT. IgG‐epitope mapping identified four distinct, non‐overlapping IgG‐binding regions on Bet v 1. Six peptides derived from these regions were successfully produced and did not induce basophil degranulation in vitro. The application of DropMap microfluidics allowed high‐resolution single B‐cell analysis, providing novel insights into allergen‐specific B‐cell responses and the effects of AIT at the clonal level.


Conclusion
This integrated approach identifies hypoallergenic peptides that selectively engage protective IgG responses and offers a framework for developing safer, next‐generation immunotherapies for allergic disease.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/a0f92660-4bbc-4a18-9301-be417d36a092/cea70276-toc-0001-m.png"
     alt="Patient-Derived IgG Epitope Mapping of Bet v 1 Reveals Hypoallergenic Peptide Candidates for Safe and Next-Generation Allergen Immunotherapy"/&gt;
&lt;p&gt;Mapping IgG epitopes of the major birch allergen Bet v 1 identified patient-derived, hypoallergenic peptides that did not trigger degranulation. These findings support a novel, safer approach for peptide-based allergen immunotherapy that leverages naturally induced IgG specificities from allergic individuals.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Allergen immunotherapy (AIT) is the only curative treatment for allergic diseases, primarily by inducing allergen-neutralising IgG antibodies. However, its use is limited by frequent allergic adverse events.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To facilitate the design of IgG-epitope-based peptide vaccines, this study aimed to identify IgG-binding regions on the major birch pollen allergen, &lt;i&gt;Bet v 1&lt;/i&gt;, using patient-derived immune profiles.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Blood samples were collected from 30 birch pollen-allergic patients, both AIT-treated and untreated; healthy individuals were included as controls. Sera were analysed for allergen-specific IgE, IgG, and IgG4, and basophil degranulation inhibition was assessed in humanised RBL cells and blood from allergic individuals. We used DropMap microfluidics for single-cell affinity profiling of IgG- and IgG4-secreting B cells. IgG epitopes were mapped using overlapping peptides and CLIPS technology. Candidate AIT peptides were synthesised on solid phase via Fmoc strategy, and their allergenicity was assessed in basophil degranulation and cellular antigen stimulation assays.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Sera from AIT-treated patients exhibited elevated IgG and IgG4 levels and enhanced inhibition of basophil degranulation. Single-cell analysis indicated IgG-affinity maturation with AIT. IgG-epitope mapping identified four distinct, non-overlapping IgG-binding regions on &lt;i&gt;Bet v 1&lt;/i&gt;. Six peptides derived from these regions were successfully produced and did not induce basophil degranulation in vitro. The application of DropMap microfluidics allowed high-resolution single B-cell analysis, providing novel insights into allergen-specific B-cell responses and the effects of AIT at the clonal level.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This integrated approach identifies hypoallergenic peptides that selectively engage protective IgG responses and offers a framework for developing safer, next-generation immunotherapies for allergic disease.&lt;/p&gt;</content:encoded>
         <dc:creator>
Lara Šošić, 
Marta Paolucci, 
Alessandro Streuli, 
David A. Melillo, 
Tianchi Jiang, 
Raffaela Campana, 
Claudia C. V. Lang, 
Thomas M. Kündig, 
Christian Steuer, 
Klaus Eyer, 
Pål Johansen
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Patient‐Derived IgG Epitope Mapping of Bet v 1 Reveals Hypoallergenic Peptide Candidates for Safe and Next‐Generation Allergen Immunotherapy</dc:title>
         <dc:identifier>10.1111/cea.70276</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70276</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70276?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70271?af=R</link>
         <pubDate>Tue, 10 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-10T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70271</guid>
         <title>Completion of the Icatibant Outcome Survey and What We Learned</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Laurence Bouillet, 
Werner Aberer, 
Teresa Caballero, 
Anete S. Grumach, 
Hilary J. Longhurst, 
Alissa Dangel, 
Natalie Khutoryansky, 
Irmgard Andresen, 
Andrea Zanichelli
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Completion of the Icatibant Outcome Survey and What We Learned</dc:title>
         <dc:identifier>10.1111/cea.70271</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70271</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70271?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70260?af=R</link>
         <pubDate>Sun, 08 Mar 2026 20:14:06 -0700</pubDate>
         <dc:date>2026-03-08T08:14:06-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70260</guid>
         <title>Global Prevalence of Sexual Dysfunction in Individuals With Atopic Dermatitis and Asthma: A Systematic Review and Meta‐Analysis</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Sexual dysfunction is an often‐overlooked aspect of allergic diseases. It was more frequently reported in asthma than in atopic dermatitis and was consistently higher among females. Estimates varied by assessment approach, highlighting the need to address sexual health and standardise evaluation methods.

ABSTRACT

Objective
Asthma and atopic dermatitis are associated with various physical and psychosocial outcomes, however, the prevalence of sexual dysfunction in these populations remains underexplored. This meta‐analysis aimed to assess the prevalence of sexual dysfunction among individuals with asthma and atopic dermatitis.


Design
A systematic review and random‐effects meta‐analysis was conducted to estimate pooled prevalence with 95% confidence intervals (CIs). Subgroup analyses were conducted stratifying by sex, geographic regions and diagnostic tools.


Data Sources
PubMed/MEDLINE, Embase, Scopus and Cochrane Library were searched from inception to 1 July 2025.


Eligibility Criteria
Studies including adults with asthma or atopic dermatitis were eligible. Sexual dysfunction was defined as impairments in sexual desire or sexual response, identified via clinical diagnosis or validated questionnaires, including the Female Sexual Function Index and International Index of Erectile Function.


Results
A total of 19 studies comprising 10,851 participants, including 1577 patients with asthma or atopic dermatitis from 18 countries across five continents, were included. The pooled prevalence of sexual dysfunction was 54.3% (95% CI 45.9–64.3) in asthma and 19.1% (13.4–27.3) in atopic dermatitis. In both conditions, prevalence was substantially higher in females than males: 71.5% (95% CI 63.3–80.7) versus 29.6% (17.1–51.2) in asthma and 53.0% (36.4–77.1) versus 16.7% (7.3–38.2) in atopic dermatitis. Studies using validated tools reported higher prevalence than those relying on supportive methods or clinical diagnoses. Smoking status was not significantly associated with differences in prevalence among individuals with asthma. Among control groups, pooled prevalence was 9.7% (95% CI 0.6–169.6) for males and 30.1% (18.7–48.5) for females in asthma studies and 2.2% (0.16–28.8) overall in atopic dermatitis studies.


Conclusions
Sexual dysfunction was highly prevalent among individuals with asthma and atopic dermatitis, particularly in females. These findings highlight the need for greater clinical attention to sexual dysfunction in the management of allergic diseases.


Systematic Review Registration
PROSPERO (CRD420251115928).

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/12fd98a7-c4a3-4969-93c5-510ac2ab8667/cea70260-toc-0001-m.png"
     alt="Global Prevalence of Sexual Dysfunction in Individuals With Atopic Dermatitis and Asthma: A Systematic Review and Meta-Analysis"/&gt;
&lt;p&gt;Sexual dysfunction is an often-overlooked aspect of allergic diseases. It was more frequently reported in asthma than in atopic dermatitis and was consistently higher among females. Estimates varied by assessment approach, highlighting the need to address sexual health and standardise evaluation methods.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;Asthma and atopic dermatitis are associated with various physical and psychosocial outcomes, however, the prevalence of sexual dysfunction in these populations remains underexplored. This meta-analysis aimed to assess the prevalence of sexual dysfunction among individuals with asthma and atopic dermatitis.&lt;/p&gt;
&lt;h2&gt;Design&lt;/h2&gt;
&lt;p&gt;A systematic review and random-effects meta-analysis was conducted to estimate pooled prevalence with 95% confidence intervals (CIs). Subgroup analyses were conducted stratifying by sex, geographic regions and diagnostic tools.&lt;/p&gt;
&lt;h2&gt;Data Sources&lt;/h2&gt;
&lt;p&gt;PubMed/MEDLINE, Embase, Scopus and Cochrane Library were searched from inception to 1 July 2025.&lt;/p&gt;
&lt;h2&gt;Eligibility Criteria&lt;/h2&gt;
&lt;p&gt;Studies including adults with asthma or atopic dermatitis were eligible. Sexual dysfunction was defined as impairments in sexual desire or sexual response, identified via clinical diagnosis or validated questionnaires, including the Female Sexual Function Index and International Index of Erectile Function.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;A total of 19 studies comprising 10,851 participants, including 1577 patients with asthma or atopic dermatitis from 18 countries across five continents, were included. The pooled prevalence of sexual dysfunction was 54.3% (95% CI 45.9–64.3) in asthma and 19.1% (13.4–27.3) in atopic dermatitis. In both conditions, prevalence was substantially higher in females than males: 71.5% (95% CI 63.3–80.7) versus 29.6% (17.1–51.2) in asthma and 53.0% (36.4–77.1) versus 16.7% (7.3–38.2) in atopic dermatitis. Studies using validated tools reported higher prevalence than those relying on supportive methods or clinical diagnoses. Smoking status was not significantly associated with differences in prevalence among individuals with asthma. Among control groups, pooled prevalence was 9.7% (95% CI 0.6–169.6) for males and 30.1% (18.7–48.5) for females in asthma studies and 2.2% (0.16–28.8) overall in atopic dermatitis studies.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Sexual dysfunction was highly prevalent among individuals with asthma and atopic dermatitis, particularly in females. These findings highlight the need for greater clinical attention to sexual dysfunction in the management of allergic diseases.&lt;/p&gt;
&lt;h2&gt;Systematic Review Registration&lt;/h2&gt;
&lt;p&gt;PROSPERO (CRD420251115928).&lt;/p&gt;</content:encoded>
         <dc:creator>
Suh Hyun Kim, 
Soeun Kim, 
Dongjin Yeo, 
Seohyun Hong, 
Yoon Lee, 
Yeona Jo, 
Seong H. Cho, 
Dong Keon Yon, 
Nikolaos G. Papadopoulos
</dc:creator>
         <category>SYSTEMATIC REVIEW</category>
         <dc:title>Global Prevalence of Sexual Dysfunction in Individuals With Atopic Dermatitis and Asthma: A Systematic Review and Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/cea.70260</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70260</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70260?af=R</prism:url>
         <prism:section>SYSTEMATIC REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70272?af=R</link>
         <pubDate>Sat, 07 Mar 2026 23:10:16 -0800</pubDate>
         <dc:date>2026-03-07T11:10:16-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70272</guid>
         <title>A Phase 1 Prognostic Trial for Predicting Paediatric Allergy Using the Placenta at Birth</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
It may be possible in the future to predict which children will develop an allergy using the placenta at birth. This will allow for early intervention to prevent the onset of the disease or reduce its impact.

ABSTRACT

Background
Allergy is the most common and earliest onset non‐communicable disease in children. The early identification of children who are at risk of allergy would allow early intervention to prevent the onset of the disease or reduce its impact. The origins of allergy are hypothesized to be derived from early developmental events which include prenatal events and early childhood exposures. We have previously identified that many placental glucocorticoid‐regulated genes were also associated with child allergy.


Objective
We have questioned if it is possible to predict which children are at risk of allergy based on their placental glucocorticoid‐regulated mRNA profile.


Methods
Placentae from two different populations located in South Australia (n = 105) and Victoria, Australia (n = 261) were included in the study. Glucocorticoid regulated genes were measured by qPCR. Statistical modelling was executed in R (version 4.4.1).


Results
Evaluation of the importance of each gene in the model identified AFF1, ARID5B, IER3, ATF4 and SLC19A2 as the top five ranking genes. The best‐performing random forest model achieved an AUC of 0.664, indicating moderate ability to distinguish between positive and negative allergic susceptibility. While our models demonstrate both measurable specificity and sensitivity, the glucocorticoid genes particularly excel at identifying children who will not develop an allergy.


Conclusion
This study demonstrates that placental glucocorticoid‐regulated genes possess significant predictive power, especially in identifying individuals unlikely to develop allergies. It offers further evidence that the placentae of nonallergic children and allergic children are transcriptionally distinct.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/68d2840f-6ea6-4899-9317-3c1e1c8ef106/cea70272-toc-0001-m.png"
     alt="A Phase 1 Prognostic Trial for Predicting Paediatric Allergy Using the Placenta at Birth"/&gt;
&lt;p&gt;It may be possible in the future to predict which children will develop an allergy using the placenta at birth. This will allow for early intervention to prevent the onset of the disease or reduce its impact.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Allergy is the most common and earliest onset non-communicable disease in children. The early identification of children who are at risk of allergy would allow early intervention to prevent the onset of the disease or reduce its impact. The origins of allergy are hypothesized to be derived from early developmental events which include prenatal events and early childhood exposures. We have previously identified that many placental glucocorticoid-regulated genes were also associated with child allergy.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;We have questioned if it is possible to predict which children are at risk of allergy based on their placental glucocorticoid-regulated mRNA profile.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Placentae from two different populations located in South Australia (&lt;i&gt;n&lt;/i&gt; = 105) and Victoria, Australia (&lt;i&gt;n&lt;/i&gt; = 261) were included in the study. Glucocorticoid regulated genes were measured by qPCR. Statistical modelling was executed in R (version 4.4.1).&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Evaluation of the importance of each gene in the model identified &lt;i&gt;AFF1&lt;/i&gt;, &lt;i&gt;ARID5B&lt;/i&gt;, &lt;i&gt;IER3&lt;/i&gt;, &lt;i&gt;ATF4&lt;/i&gt; and &lt;i&gt;SLC19A2&lt;/i&gt; as the top five ranking genes. The best-performing random forest model achieved an AUC of 0.664, indicating moderate ability to distinguish between positive and negative allergic susceptibility. While our models demonstrate both measurable specificity and sensitivity, the glucocorticoid genes particularly excel at identifying children who will not develop an allergy.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study demonstrates that placental glucocorticoid-regulated genes possess significant predictive power, especially in identifying individuals unlikely to develop allergies. It offers further evidence that the placentae of nonallergic children and allergic children are transcriptionally distinct.&lt;/p&gt;</content:encoded>
         <dc:creator>
Vicki L. Clifton, 
Zarqa Saif, 
Ana Patricia Balbon, 
Muhammad Afnan, 
Andrew Tai, 
Sailesh Kumar, 
Janet M. Davies, 
Peter D. Sly, 
Jane Peake, 
Richard Saffery, 
Peter J. Vuillermin, 
BIS Investigator Group, 
Brian Cox
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>A Phase 1 Prognostic Trial for Predicting Paediatric Allergy Using the Placenta at Birth</dc:title>
         <dc:identifier>10.1111/cea.70272</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70272</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70272?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70269?af=R</link>
         <pubDate>Fri, 06 Mar 2026 22:15:13 -0800</pubDate>
         <dc:date>2026-03-06T10:15:13-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70269</guid>
         <title>Quality and Consistency of Penicillin Allergy Delabelling Guidelines: A Systematic Review</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Eighteen penicillin allergy delabelling guidelines from 12 countries were reviewed. There is consensus for staged risk‐based testing, with emerging support for direct oral challenge in low‐risk patients and expanded non‐specialist roles. Overall guideline quality was low, with major gaps in methodological rigour, stakeholder involvement, and implementation strategies.

ABSTRACT

Objective and Design
This systematic review compared the scope, purpose, and recommendations of internationally published penicillin allergy delabelling guidelines (PADLGs) and assessed their quality using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument.


Data Sources
A systematic search of MEDLINE, EMBASE, and CINAHL databases, and Google, Google Scholar, websites of professional allergy societies (n = 95), and guideline repositories (n = 16) was conducted to August 2024.


Eligibility Criteria
Any document that reported itself as being an evidence‐based guideline, practice guideline, expert recommendation, consensus statement, position paper, or practice parameter for penicillin allergy delabelling (‘PADL‐G’) was eligible for inclusion. Only those developed for use by health care professionals were included. Guidelines for community or patient use and hospital protocols or fact sheets were excluded.


Results
Eighteen guidelines published between 2014 and 2024 were identified, representing 12 countries across four regions. PADLGs varied in scope, target users, and clinical recommendations, both within and across clinical settings. Most provided recommendations for risk stratification, testing, and delabelling methods, with many supporting direct delabelling/direct challenge in low‐risk patients. Substantial variation was observed in risk assessment tools, eligibility criteria, and post‐test delabelling strategies. Overall, the quality of PADLGs was low, with only two meeting predefined high‐quality criteria. Critical gaps included limited methodological rigour, poor stakeholder involvement, and lack of guidance for real‐world implementation.


Conclusions
To support safe and scalable PADL approaches, clearer, more consistent, and methodologically robust guidelines are needed to address the global burden of inappropriate penicillin allergy labels.


Systematic Review Registration
The protocol for this review was prospectively registered at Open Science Framework: osf.io/9fvr7.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/7a7f65d0-ef16-42af-8cc8-27304b507750/cea70269-toc-0001-m.png"
     alt="Quality and Consistency of Penicillin Allergy Delabelling Guidelines: A Systematic Review"/&gt;
&lt;p&gt;Eighteen penicillin allergy delabelling guidelines from 12 countries were reviewed. There is consensus for staged risk-based testing, with emerging support for direct oral challenge in low-risk patients and expanded non-specialist roles. Overall guideline quality was low, with major gaps in methodological rigour, stakeholder involvement, and implementation strategies.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective and Design&lt;/h2&gt;
&lt;p&gt;This systematic review compared the scope, purpose, and recommendations of internationally published penicillin allergy delabelling guidelines (PADLGs) and assessed their quality using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument.&lt;/p&gt;
&lt;h2&gt;Data Sources&lt;/h2&gt;
&lt;p&gt;A systematic search of MEDLINE, EMBASE, and CINAHL databases, and Google, Google Scholar, websites of professional allergy societies (&lt;i&gt;n&lt;/i&gt; = 95), and guideline repositories (&lt;i&gt;n&lt;/i&gt; = 16) was conducted to August 2024.&lt;/p&gt;
&lt;h2&gt;Eligibility Criteria&lt;/h2&gt;
&lt;p&gt;Any document that reported itself as being an evidence-based guideline, practice guideline, expert recommendation, consensus statement, position paper, or practice parameter for penicillin allergy delabelling (‘PADL-G’) was eligible for inclusion. Only those developed for use by health care professionals were included. Guidelines for community or patient use and hospital protocols or fact sheets were excluded.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Eighteen guidelines published between 2014 and 2024 were identified, representing 12 countries across four regions. PADLGs varied in scope, target users, and clinical recommendations, both within and across clinical settings. Most provided recommendations for risk stratification, testing, and delabelling methods, with many supporting direct delabelling/direct challenge in low-risk patients. Substantial variation was observed in risk assessment tools, eligibility criteria, and post-test delabelling strategies. Overall, the quality of PADLGs was low, with only two meeting predefined high-quality criteria. Critical gaps included limited methodological rigour, poor stakeholder involvement, and lack of guidance for real-world implementation.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;To support safe and scalable PADL approaches, clearer, more consistent, and methodologically robust guidelines are needed to address the global burden of inappropriate penicillin allergy labels.&lt;/p&gt;
&lt;h2&gt;Systematic Review Registration&lt;/h2&gt;
&lt;p&gt;The protocol for this review was prospectively registered at Open Science Framework: &lt;a target="_blank"
   title="Link to external resource"
   href="http://osf.io/9fvr7"&gt;osf.io/9fvr7&lt;/a&gt;.&lt;/p&gt;</content:encoded>
         <dc:creator>
Jessie He, 
Marina Guirguis, 
Sankare Devanandan, 
Rani Scott‐Farmer, 
Sandra Vale, 
Michaela Lucas, 
Jennifer J. Koplin, 
Catherine J. Hornung, 
Sandra M. Salter
</dc:creator>
         <category>SYSTEMATIC REVIEW</category>
         <dc:title>Quality and Consistency of Penicillin Allergy Delabelling Guidelines: A Systematic Review</dc:title>
         <dc:identifier>10.1111/cea.70269</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70269</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70269?af=R</prism:url>
         <prism:section>SYSTEMATIC REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70273?af=R</link>
         <pubDate>Fri, 06 Mar 2026 21:59:00 -0800</pubDate>
         <dc:date>2026-03-06T09:59:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70273</guid>
         <title>Global Variation in Anaphylaxis Treatment: A Scoping Review Protocol</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ayel Luis R. Batac, 
Andrew Wong‐Pack, 
Mê‐Linh Lê, 
Justine Claire R. Reyes, 
Manvir K. Bhamra, 
Billy Hong, 
Laura Y. Feldman, 
Andrew T. Fong, 
Philippe Bégin
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Global Variation in Anaphylaxis Treatment: A Scoping Review Protocol</dc:title>
         <dc:identifier>10.1111/cea.70273</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70273</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70273?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70268?af=R</link>
         <pubDate>Fri, 06 Mar 2026 21:54:40 -0800</pubDate>
         <dc:date>2026-03-06T09:54:40-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70268</guid>
         <title>Association Between Asthma Biologics and Risk of Herpes Zoster Among US Adults With Asthma: A Pairwise Comparison</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Chun‐Tse Hung, 
Chen‐Yen An, 
Jun Gong, 
Chi‐Won Suk, 
Yuarn‐Jang Lee, 
Shun‐Hsing Hung
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Association Between Asthma Biologics and Risk of Herpes Zoster Among US Adults With Asthma: A Pairwise Comparison</dc:title>
         <dc:identifier>10.1111/cea.70268</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70268</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70268?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70241?af=R</link>
         <pubDate>Thu, 05 Mar 2026 16:14:58 -0800</pubDate>
         <dc:date>2026-03-05T04:14:58-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70241</guid>
         <title>Impact of Oral Sebetralstat on Anxiety Associated With Hereditary Angioedema Attacks</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
In the phase 3 KONFIDENT trial of oral sebetralstat for on‐demand treatment of hereditary angioedema attacks, many attacks induced moderate‐to‐extreme anxiety. Sebetralstat reduced anxiety versus placebo; time to reductions agreed with trial endpoints, such as time to beginning of symptom relief. These results suggest that sebetralstat can play a role in alleviating attack‐related anxiety in people living with hereditary angioedema. GA‐NRS, General Anxiety Numeric Rating Scale; HAE, hereditary angioedema.

ABSTRACT

Background
People with hereditary angioedema (HAE) experience anxiety from the unpredictable nature of attacks and the burden of parenteral on‐demand therapies, potentially leading to delays or avoidance of treatment. This analysis assessed factors associated with anxiety during attacks and the impact of oral sebetralstat versus placebo on anxiety in the KONFIDENT trial.


Methods
Participants in the randomised, double‐blind, phase 3 KONFIDENT trial (NCT05259917) treated attacks with sebetralstat 300 mg, 600 mg or placebo as early as possible after onset. Anxiety was recorded at treatment administration, every 0.5 h thereafter through 4 h, hourly from 5 to 12 h and every 2 h from 14 to 24 h using an 11‐point modified General Anxiety Numeric Rating Scale (GA‐NRS). Prespecified exploratory endpoints assessed in all attacks and in attacks rated as inducing moderate‐to‐extreme anxiety (GA‐NRS ≥ 4) included cumulative GA‐NRS score and meaningful reduction in anxiety (defined as ≥ 2‐point reduction in GA‐NRS for ≥ 2 consecutive timepoints); least squares mean change from treatment administration in GA‐NRS at 4 and 12 h was also assessed. This study was sponsored by KalVista Pharmaceuticals.


Results
Overall, 115 (44%) attacks were rated as inducing moderate‐to‐extreme anxiety. Female sex, shorter time since HAE diagnosis and greater attack severity were associated with greater anxiety at treatment administration. Reduction in cumulative anxiety after sebetralstat use was significantly greater versus placebo. The time to meaningful reduction in anxiety endpoint showed agreement with time to beginning of symptom relief, reduction in attack severity and complete attack resolution endpoints.


Conclusion
Moderate‐to‐extreme anxiety was common in HAE attacks. Reduction in anxiety was significantly greater in attacks treated with sebetralstat compared with placebo.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/5abb8da3-75e5-4a2a-b060-2f345033c551/cea70241-toc-0001-m.png"
     alt="Impact of Oral Sebetralstat on Anxiety Associated With Hereditary Angioedema Attacks"/&gt;
&lt;p&gt;In the phase 3 KONFIDENT trial of oral sebetralstat for on-demand treatment of hereditary angioedema attacks, many attacks induced moderate-to-extreme anxiety. Sebetralstat reduced anxiety versus placebo; time to reductions agreed with trial endpoints, such as time to beginning of symptom relief. These results suggest that sebetralstat can play a role in alleviating attack-related anxiety in people living with hereditary angioedema. GA-NRS, General Anxiety Numeric Rating Scale; HAE, hereditary angioedema.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;People with hereditary angioedema (HAE) experience anxiety from the unpredictable nature of attacks and the burden of parenteral on-demand therapies, potentially leading to delays or avoidance of treatment. This analysis assessed factors associated with anxiety during attacks and the impact of oral sebetralstat versus placebo on anxiety in the KONFIDENT trial.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Participants in the randomised, double-blind, phase 3 KONFIDENT trial (NCT05259917) treated attacks with sebetralstat 300 mg, 600 mg or placebo as early as possible after onset. Anxiety was recorded at treatment administration, every 0.5 h thereafter through 4 h, hourly from 5 to 12 h and every 2 h from 14 to 24 h using an 11-point modified General Anxiety Numeric Rating Scale (GA-NRS). Prespecified exploratory endpoints assessed in all attacks and in attacks rated as inducing moderate-to-extreme anxiety (GA-NRS ≥ 4) included cumulative GA-NRS score and meaningful reduction in anxiety (defined as ≥ 2-point reduction in GA-NRS for ≥ 2 consecutive timepoints); least squares mean change from treatment administration in GA-NRS at 4 and 12 h was also assessed. This study was sponsored by KalVista Pharmaceuticals.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Overall, 115 (44%) attacks were rated as inducing moderate-to-extreme anxiety. Female sex, shorter time since HAE diagnosis and greater attack severity were associated with greater anxiety at treatment administration. Reduction in cumulative anxiety after sebetralstat use was significantly greater versus placebo. The time to meaningful reduction in anxiety endpoint showed agreement with time to beginning of symptom relief, reduction in attack severity and complete attack resolution endpoints.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Moderate-to-extreme anxiety was common in HAE attacks. Reduction in anxiety was significantly greater in attacks treated with sebetralstat compared with placebo.&lt;/p&gt;</content:encoded>
         <dc:creator>
Timothy Craig, 
Emel Aygören‐Pürsün, 
Jonathan A. Bernstein, 
Paula J. Busse, 
Teresa Caballero, 
Danny M. Cohn, 
Mar Guilarte, 
Henriette Farkas, 
Douglas H. Jones, 
Sorena Kiani‐Alikhan, 
Michael E. Manning, 
Marcus Maurer, 
Marc A. Riedl, 
Sinisa Savic, 
H. James Wedner, 
Patrick F. K. Yong, 
Andrea Zanichelli, 
Sally van Kooten, 
Matthew Iverson, 
Erik Hansen, 
James Hao, 
Michael D. Smith, 
Christopher M. Yea, 
Paul K. Audhya, 
William R. Lumry
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Impact of Oral Sebetralstat on Anxiety Associated With Hereditary Angioedema Attacks</dc:title>
         <dc:identifier>10.1111/cea.70241</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70241</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70241?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70261?af=R</link>
         <pubDate>Thu, 26 Feb 2026 17:54:59 -0800</pubDate>
         <dc:date>2026-02-26T05:54:59-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70261</guid>
         <title>A Pilot Randomised Controlled Dose‐Ranging Trial of Ant Venom Immunotherapy With and Without Delta‐Inulin Adjuvant</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Low dose (25mcg) jack jumper ant venom immunotherapy with or without Advax adjuvant, had similar efficacy to the current standard of care. Reduction in basophil activation test reactivity in response to treatment correlated with sting challenge outcome.

ABSTRACT

Introduction
Jack Jumper ant (JJA) venom immunotherapy (VIT) is highly efficacious but the lowest effective dose is unknown. Delta‐inulin adjuvant (Advax) is known to enhance honeybee VIT immunogenicity.


Objective
This phase 1/2 single‐blind, randomised controlled trial aimed to compare the efficacy and safety of JJA VIT with different doses of venom ± Advax.


Methods
Adults aged 18–65 with a history of immediate systemic reaction (SR) to JJA stings were randomised to receive JJA VIT at a maintenance dose of 25 mcg or 50 mcg ± Advax; participants were blinded to treatment allocation. Primary outcomes were the response to sting challenges after 12 months and venom‐specific IgE and IgG4 responses to treatment.


Results
Forty‐nine of 50 screened subjects met inclusion criteria and were randomised; 44 started treatment (25 mcg n = 12; 25 mcg + Advax n = 13; 50mcg n = 12, 50 mcg + Advax n = 12). Subsequently, two withdrew due to SRs to treatment, and two withdrew due to unrelated factors. The higher JJA venom maintenance dose was associated with reduced likelihood of SRs (OR 0.53 (95% CI, 0.28–0.98)), while Advax did not have an effect (OR 1.17 (95% CI, 0.59–2.32)). Forty proceeded to sting challenge, with six developing SRs. There was no difference between groups for sting challenge outcome (p = 0.98), and the ORs for 25 mcg vs. 50 mcg venom dose (0.89, 95% CI, 0.38–2.09) and Advax vs. no Advax (0.99, 95% CI 0.42–2.33) indicated no effect. There were no differences between groups for venom sIgE (p = 0.78), sIgG4 (p = 0.25), sIgE/IgG4 ratio (p = 0.42), intradermal (p = 0.77), and basophil activation test (BAT) (p = 0.69) responses to treatment. Subjects with high baseline BAT sensitivity, which reduced markedly in response to treatment, were less likely to have a positive sting challenge (p = 0.006).


Conclusion
Challenge outcomes were similar for all groups, with no significant difference found between 25 and 50 mcg maintenance dose or between treatment with and without Advax. Further research of low dose JJA VIT is warranted to confirm its efficacy and tolerability.


Trial Registration
NCT03066986

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/bcbed7a5-e6c7-4534-bf0f-b8bd322c526e/cea70261-toc-0001-m.png"
     alt="A Pilot Randomised Controlled Dose-Ranging Trial of Ant Venom Immunotherapy With and Without Delta-Inulin Adjuvant"/&gt;
&lt;p&gt;Low dose (25mcg) jack jumper ant venom immunotherapy with or without Advax adjuvant, had similar efficacy to the current standard of care. Reduction in basophil activation test reactivity in response to treatment correlated with sting challenge outcome.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Jack Jumper ant (JJA) venom immunotherapy (VIT) is highly efficacious but the lowest effective dose is unknown. Delta-inulin adjuvant (Advax) is known to enhance honeybee VIT immunogenicity.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This phase 1/2 single-blind, randomised controlled trial aimed to compare the efficacy and safety of JJA VIT with different doses of venom ± Advax.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Adults aged 18–65 with a history of immediate systemic reaction (SR) to JJA stings were randomised to receive JJA VIT at a maintenance dose of 25 mcg or 50 mcg ± Advax; participants were blinded to treatment allocation. Primary outcomes were the response to sting challenges after 12 months and venom-specific IgE and IgG4 responses to treatment.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Forty-nine of 50 screened subjects met inclusion criteria and were randomised; 44 started treatment (25 mcg &lt;i&gt;n&lt;/i&gt; = 12; 25 mcg + Advax &lt;i&gt;n&lt;/i&gt; = 13; 50mcg &lt;i&gt;n&lt;/i&gt; = 12, 50 mcg + Advax &lt;i&gt;n&lt;/i&gt; = 12). Subsequently, two withdrew due to SRs to treatment, and two withdrew due to unrelated factors. The higher JJA venom maintenance dose was associated with reduced likelihood of SRs (OR 0.53 (95% CI, 0.28–0.98)), while Advax did not have an effect (OR 1.17 (95% CI, 0.59–2.32)). Forty proceeded to sting challenge, with six developing SRs. There was no difference between groups for sting challenge outcome (&lt;i&gt;p&lt;/i&gt; = 0.98), and the ORs for 25 mcg vs. 50 mcg venom dose (0.89, 95% CI, 0.38–2.09) and Advax vs. no Advax (0.99, 95% CI 0.42–2.33) indicated no effect. There were no differences between groups for venom sIgE (&lt;i&gt;p&lt;/i&gt; = 0.78), sIgG4 (&lt;i&gt;p&lt;/i&gt; = 0.25), sIgE/IgG4 ratio (&lt;i&gt;p&lt;/i&gt; = 0.42), intradermal (&lt;i&gt;p&lt;/i&gt; = 0.77), and basophil activation test (BAT) (&lt;i&gt;p&lt;/i&gt; = 0.69) responses to treatment. Subjects with high baseline BAT sensitivity, which reduced markedly in response to treatment, were less likely to have a positive sting challenge (&lt;i&gt;p&lt;/i&gt; = 0.006).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Challenge outcomes were similar for all groups, with no significant difference found between 25 and 50 mcg maintenance dose or between treatment with and without Advax. Further research of low dose JJA VIT is warranted to confirm its efficacy and tolerability.&lt;/p&gt;
&lt;h2&gt;Trial Registration&lt;/h2&gt;
&lt;p&gt;NCT03066986&lt;/p&gt;</content:encoded>
         <dc:creator>
Thanh‐Thao Adriana Le, 
Troy Wanandy, 
Griffith B. Perkins, 
Susan Lester, 
Wun Yee Lau, 
Malcolm Turner, 
Richard J. Woodman, 
Emily M. Mulcahy, 
Sherin Vareeckal Joseph, 
Shweta Mhatre, 
Simon G. A. Brown, 
Michael D. Wiese, 
Nikolai Petrovsky, 
Robert J. Heddle, 
Pravin Hissaria
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>A Pilot Randomised Controlled Dose‐Ranging Trial of Ant Venom Immunotherapy With and Without Delta‐Inulin Adjuvant</dc:title>
         <dc:identifier>10.1111/cea.70261</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70261</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70261?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70267?af=R</link>
         <pubDate>Thu, 26 Feb 2026 17:35:07 -0800</pubDate>
         <dc:date>2026-02-26T05:35:07-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70267</guid>
         <title>Allergic Diseases and Triglyceride‐Related Lipid Profiles in Nationally Representative Korean Adults</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Yu Kyoung Hwang, 
Hyo‐Jin Min
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Allergic Diseases and Triglyceride‐Related Lipid Profiles in Nationally Representative Korean Adults</dc:title>
         <dc:identifier>10.1111/cea.70267</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70267</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70267?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70264?af=R</link>
         <pubDate>Wed, 25 Feb 2026 19:19:48 -0800</pubDate>
         <dc:date>2026-02-25T07:19:48-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70264</guid>
         <title>Diverging in Vivo Immune Response Patterns After Oral Food Challenge in Peanut Allergic Adults</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
After the oral food challenge, peanut (PN)‐allergic adults were monitored over 4 weeks, which revealed diverging immune response patterns, with strong responders (SR) exhibiting heightened Ara h 2+ B cell expansion, PN sIgE induction and increasing PN‐specific Tconv. Weak responders (WR) had more activated PN‐specific Tregs. This variability in the immune response may have clinical implications.

ABSTRACT

Background
Peanut (PN) allergy is an IgE‐mediated hypersensitivity with a deviated adaptive immune response dominated by IgE‐producing B cells and type 2 T cells (Th2). The in vivo immune response upon antigen encounter, for example, after oral food challenge (OFC), has not been investigated over prolonged timeframes.


Methods
Here, we investigated the kinetics of allergen‐specific adaptive immune responses in PN‐allergic and non‐allergic adults before OFC (d0) and thereafter at d7, d14, d21, d28 by determining PN‐specific CD40L+4‐1BB+ conventional (Tconv) and FoxP3+ Helios+ CD40L−4‐1BB+ regulatory T cells (Treg), Ara h 2‐specific B cells and PN‐specific sIgE and sIgG4 antibody levels.


Results
In PN‐allergic donors, PN sIgE levels increased until d28 after OFC, but to a variable extent. This variability was associated with a differential increase of Ara h 2+ B cells at d7, based on which we identified strong and weak responders (SR and WR). SR exhibited a more pronounced increase of PN sIgE, stronger in vivo activation of T and B cells (HLA‐DR+, Ki‐67+, CD21−), as well as prominent induction of the low‐affinity IgE receptor CD23 in Ara h 2+ B cells. In contrast, WR exhibited strong activation of PN‐specific Tregs at d7. At baseline, SR and WR differed regarding Ara h 2+ memory B cells and frequencies of Th2 and type 2‐driving Helios‐expressing PN‐specific Tconv. Minor changes in Th1 cells were also observed in non‐allergic donors.


Conclusions
Our results indicate differential adaptive immune responses towards OFC in PN‐allergic adults. In summary, SR displayed a more allergy‐maintaining immune response, while WR displayed a rather suppressive immune response. Underlying responsible factors such as genetics, as well as clinical consequences, will require further investigation in larger cohorts.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/348ae6c5-be47-4e4a-b755-8d5dad10fe58/cea70264-toc-0001-m.png"
     alt="Diverging in Vivo Immune Response Patterns After Oral Food Challenge in Peanut Allergic Adults"/&gt;
&lt;p&gt;After the oral food challenge, peanut (PN)-allergic adults were monitored over 4 weeks, which revealed diverging immune response patterns, with strong responders (SR) exhibiting heightened Ara h 2&lt;sup&gt;+&lt;/sup&gt; B cell expansion, PN sIgE induction and increasing PN-specific Tconv. Weak responders (WR) had more activated PN-specific Tregs. This variability in the immune response may have clinical implications.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Peanut (PN) allergy is an IgE-mediated hypersensitivity with a deviated adaptive immune response dominated by IgE-producing B cells and type 2 T cells (Th2). The in vivo immune response upon antigen encounter, for example, after oral food challenge (OFC), has not been investigated over prolonged timeframes.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Here, we investigated the kinetics of allergen-specific adaptive immune responses in PN-allergic and non-allergic adults before OFC (d0) and thereafter at d7, d14, d21, d28 by determining PN-specific CD40L&lt;sup&gt;+&lt;/sup&gt;4-1BB&lt;sup&gt;+&lt;/sup&gt; conventional (Tconv) and FoxP3&lt;sup&gt;+&lt;/sup&gt; Helios&lt;sup&gt;+&lt;/sup&gt; CD40L&lt;sup&gt;−&lt;/sup&gt;4-1BB&lt;sup&gt;+&lt;/sup&gt; regulatory T cells (Treg), Ara h 2-specific B cells and PN-specific sIgE and sIgG4 antibody levels.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;In PN-allergic donors, PN sIgE levels increased until d28 after OFC, but to a variable extent. This variability was associated with a differential increase of Ara h 2&lt;sup&gt;+&lt;/sup&gt; B cells at d7, based on which we identified strong and weak responders (SR and WR). SR exhibited a more pronounced increase of PN sIgE, stronger in vivo activation of T and B cells (HLA-DR&lt;sup&gt;+&lt;/sup&gt;, Ki-67&lt;sup&gt;+&lt;/sup&gt;, CD21&lt;sup&gt;−&lt;/sup&gt;), as well as prominent induction of the low-affinity IgE receptor CD23 in Ara h 2&lt;sup&gt;+&lt;/sup&gt; B cells. In contrast, WR exhibited strong activation of PN-specific Tregs at d7. At baseline, SR and WR differed regarding Ara h 2&lt;sup&gt;+&lt;/sup&gt; memory B cells and frequencies of Th2 and type 2-driving Helios-expressing PN-specific Tconv. Minor changes in Th1 cells were also observed in non-allergic donors.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Our results indicate differential adaptive immune responses towards OFC in PN-allergic adults. In summary, SR displayed a more allergy-maintaining immune response, while WR displayed a rather suppressive immune response. Underlying responsible factors such as genetics, as well as clinical consequences, will require further investigation in larger cohorts.&lt;/p&gt;</content:encoded>
         <dc:creator>
Florent Fauchère, 
Aikaterina Alexiou, 
Veronika Höfer, 
Kirsten Beyer, 
Sabine Dölle‐Bierke, 
Andreas Thiel, 
Margitta Worm, 
Julian Braun
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Diverging in Vivo Immune Response Patterns After Oral Food Challenge in Peanut Allergic Adults</dc:title>
         <dc:identifier>10.1111/cea.70264</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70264</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70264?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70265?af=R</link>
         <pubDate>Wed, 25 Feb 2026 17:59:15 -0800</pubDate>
         <dc:date>2026-02-25T05:59:15-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70265</guid>
         <title>When Biology Meets Morphology: The Clinical Counterpart of Eosinophil Extracellular Traps in Nasal Cytology</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Matteo Gelardi
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>When Biology Meets Morphology: The Clinical Counterpart of Eosinophil Extracellular Traps in Nasal Cytology</dc:title>
         <dc:identifier>10.1111/cea.70265</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70265</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70265?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70248?af=R</link>
         <pubDate>Wed, 25 Feb 2026 17:55:12 -0800</pubDate>
         <dc:date>2026-02-25T05:55:12-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70248</guid>
         <title>Body Mass Index Is Not Associated With Cough, Laryngeal Hypersensitivity or Dyspnoea in Patients With Refractory Chronic Cough: A Cross‐Sectional Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Tina Wilkie, 
Phoebe Blakey, 
Anne Vertigan
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Body Mass Index Is Not Associated With Cough, Laryngeal Hypersensitivity or Dyspnoea in Patients With Refractory Chronic Cough: A Cross‐Sectional Study</dc:title>
         <dc:identifier>10.1111/cea.70248</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70248</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70248?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70262?af=R</link>
         <pubDate>Mon, 23 Feb 2026 16:14:25 -0800</pubDate>
         <dc:date>2026-02-23T04:14:25-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70262</guid>
         <title>IgG‐Related Neutrophil Activation Is a Novel Mechanism That Defines a New Type of Immediate Hypersensitivity Reactions (IHR) to Beta‐Lactam</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Jean‐Louis Guéant, 
Adrienne Astrid Gallizzi, 
Rosa‐Maria Guéant‐Rodriguez, 
Antonino Romano, 
Jose‐Julio Laguna
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>IgG‐Related Neutrophil Activation Is a Novel Mechanism That Defines a New Type of Immediate Hypersensitivity Reactions (IHR) to Beta‐Lactam</dc:title>
         <dc:identifier>10.1111/cea.70262</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70262</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70262?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70249?af=R</link>
         <pubDate>Sun, 22 Feb 2026 20:15:11 -0800</pubDate>
         <dc:date>2026-02-22T08:15:11-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70249</guid>
         <title>Variants in Genes Encoding Innate Lymphoid Cells Type 2 Surface Markers Affecting Asthma and Atopy Pathologies</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Raphael Chagas Silva, 
Gabriela Pimentel Pinheiro, 
Hátilla dos Santos Silva, 
Talita dos Santos de Jesus, 
Carolina Melo Orrico‐Ferreira, 
Jamille Souza Fernandes Chiarelotto, 
Cinthia Vila Nova Santana, 
Carina da Silva Pinheiro, 
Ricardo Riccio Oliveira, 
Álvaro Augusto Cruz, 
Kathleen C. Barnes, 
Neuza Maria A. Neves, 
Ryan dos Santos Costa, 
Camila Alexandrina Figueiredo
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Variants in Genes Encoding Innate Lymphoid Cells Type 2 Surface Markers Affecting Asthma and Atopy Pathologies</dc:title>
         <dc:identifier>10.1111/cea.70249</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70249</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70249?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70252?af=R</link>
         <pubDate>Thu, 19 Feb 2026 19:29:48 -0800</pubDate>
         <dc:date>2026-02-19T07:29:48-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70252</guid>
         <title>Clinical Experience With Apoica pallens Venom Allergy Supports Recent Allergomic Findings</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Selsabil Ayeb, 
Jean‐Luc Bourrain
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>Clinical Experience With Apoica pallens Venom Allergy Supports Recent Allergomic Findings</dc:title>
         <dc:identifier>10.1111/cea.70252</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70252</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70252?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70263?af=R</link>
         <pubDate>Thu, 19 Feb 2026 16:50:25 -0800</pubDate>
         <dc:date>2026-02-19T04:50:25-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70263</guid>
         <title>Reply to ‘Letter to the Editor‐Re: Sabouraud‐Leclerc D, Mariotte D, Bradatan E, et al. Eight Food Allergens Without Mandatory Labelling Highlighted by the French Allergy‐Vigilance Network’</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Dominique Sabouraud‐Leclerc, 
Delphine Mariotte, 
Elena Bradatan, 
Amandine Divaret‐Chauveau, 
Carine Metz‐Favre, 
Pascale Beaumont, 
Pascale Dumond, 
Julien Serrier, 
Yasemin Karaca‐Altintas, 
Sélina Tscheiller, 
Xavier Van der Brempt, 
Guillaume Pouessel
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>Reply to ‘Letter to the Editor‐Re: Sabouraud‐Leclerc D, Mariotte D, Bradatan E, et al. Eight Food Allergens Without Mandatory Labelling Highlighted by the French Allergy‐Vigilance Network’</dc:title>
         <dc:identifier>10.1111/cea.70263</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70263</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70263?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70250?af=R</link>
         <pubDate>Thu, 19 Feb 2026 16:40:18 -0800</pubDate>
         <dc:date>2026-02-19T04:40:18-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70250</guid>
         <title>Effects of Acupuncture as a Therapeutic Intervention Targeting Both Skin and Gastrointestinal Symptoms in Patients With Atopic Dermatitis: A Randomised Controlled Trial</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Jundong Kim, 
Yerin Seo, 
Mijung Yeom, 
Su‐Yang Park, 
Sujin Lee, 
Sora Ahn, 
Dae‐Hyun Hahm, 
Soon‐Kyeong Kwon, 
Kyuseok Kim, 
Hi‐Joon Park
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Effects of Acupuncture as a Therapeutic Intervention Targeting Both Skin and Gastrointestinal Symptoms in Patients With Atopic Dermatitis: A Randomised Controlled Trial</dc:title>
         <dc:identifier>10.1111/cea.70250</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70250</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70250?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70243?af=R</link>
         <pubDate>Wed, 18 Feb 2026 19:01:10 -0800</pubDate>
         <dc:date>2026-02-18T07:01:10-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70243</guid>
         <title>Prognostic Value of Combining Serum Tryptase and Bone Mineral Density in Predicting Fractures in Systemic Mastocytosis</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
François Robin, 
Victoria Bureau, 
Antoine Vivier, 
Edwige Le Mouel, 
Sophie Besnard, 
Alain Lescoat, 
Pascal Guggenbuhl
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Prognostic Value of Combining Serum Tryptase and Bone Mineral Density in Predicting Fractures in Systemic Mastocytosis</dc:title>
         <dc:identifier>10.1111/cea.70243</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70243</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70243?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70245?af=R</link>
         <pubDate>Wed, 18 Feb 2026 18:58:22 -0800</pubDate>
         <dc:date>2026-02-18T06:58:22-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70245</guid>
         <title>Dual GIPR and GLP‐1R Agonist Tirzepatide Is Associated With Fewer Asthma Exacerbations in Adults With Obesity</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Syona Mehta, 
Syed Fahad Gillani, 
Rawan Elkomi, 
Miriam Michael
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Dual GIPR and GLP‐1R Agonist Tirzepatide Is Associated With Fewer Asthma Exacerbations in Adults With Obesity</dc:title>
         <dc:identifier>10.1111/cea.70245</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70245</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70245?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70253?af=R</link>
         <pubDate>Wed, 18 Feb 2026 00:00:00 -0800</pubDate>
         <dc:date>2026-02-18T12:00:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70253</guid>
         <title>Two Distinct Transcriptional Subtypes of Severe Type 2 Asthma in NSAID‐Exacerbated Respiratory Disease</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
The study included 27 patients with N‐ERD and severe asthma. A cluster analysis with 116 variables was performed. Two clusters were identified: cluster 1 (n = 10), T2‐low with low sputum GATA3 expression and cluster 2 (n = 17), T2‐high with high sputum GATA3 expression. Patients in cluster 1 had increased blood neutrophil count and percentage, increased sputum eosinophil count and percentage, lower sputum macrophage count and percentage and increased PGD2 in induced sputum supernatant. GATA3, transcription factor guanine adenine thymine adenine sequence‐binding protein 3; IS, induced sputum; ISS, induced sputum supernatant; N‐ERD, nonsteroidal anti‐inflammatory drug‐exacerbated respiratory disease; PGD2, prostaglandin D2.

ABSTRACT

Background
Previous studies demonstrated the heterogeneity of the nonsteroidal anti‐inflammatory drug‐exacerbated respiratory disease (N‐ERD) phenotype. Patients with severe asthma and aspirin hypersensitivity may exhibit differences in sputum mRNA gene expression. The aim of the study was to identify distinct transcriptional subtypes of severe asthma with aspirin hypersensitivity using unsupervised cluster analysis.


Methods
Sputum induction was performed in 27 patients with severe asthma and aspirin hypersensitivity who met 2022 Global Initiative for Asthma criteria for type 2 (T2) severe asthma. Using the transcriptional signatures of 87 genes, along with clinical characteristics and biomarker measurements, 2 distinct subtypes were identified and compared between study participants.


Results
Two clusters were identified: cluster 1 (n = 10) and cluster 2 (n = 17). In cluster 1, low GATA3 expression was observed, along with several activated inflammatory genes, while cluster 2 was characterised by high GATA3 expression. Cluster 1 was characterised by increased sputum eosinophil count (p = 0.04) and percentage (p = 0.035), and decreased sputum macrophage count (p = 0.003) and percentage (p = 0.003). Patients in cluster 1 had increased sputum supernatant prostaglandin D2 levels (p = 0.031). Patients in cluster 1 tended to have a higher Lund‐Mackay score (p = 0.074) and elevated peripheral blood eosinophilia (p = 0.059).


Conclusion
Patients in cluster 1 exhibited T2 inflammation with low GATA3 expression, while those in cluster 2 showed T2 inflammation with high GATA3 expression. Sputum GATA3 expression may serve as a useful biomarker for differentiating distinct severe asthma subtypes in patients with N‐ERD.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/24a4503a-af05-49e7-a186-4d0397545280/cea70253-toc-0001-m.png"
     alt="Two Distinct Transcriptional Subtypes of Severe Type 2 Asthma in NSAID-Exacerbated Respiratory Disease"/&gt;
&lt;p&gt;The study included 27 patients with N-ERD and severe asthma. A cluster analysis with 116 variables was performed. Two clusters were identified: cluster 1 (&lt;i&gt;n&lt;/i&gt; = 10), T2-low with low sputum &lt;i&gt;GATA3&lt;/i&gt; expression and cluster 2 (&lt;i&gt;n&lt;/i&gt; = 17), T2-high with high sputum &lt;i&gt;GATA3&lt;/i&gt; expression. Patients in cluster 1 had increased blood neutrophil count and percentage, increased sputum eosinophil count and percentage, lower sputum macrophage count and percentage and increased PGD&lt;sub&gt;2&lt;/sub&gt; in induced sputum supernatant. &lt;i&gt;GATA3&lt;/i&gt;, transcription factor guanine adenine thymine adenine sequence-binding protein 3; IS, induced sputum; ISS, induced sputum supernatant; N-ERD, nonsteroidal anti-inflammatory drug-exacerbated respiratory disease; PGD&lt;sub&gt;2&lt;/sub&gt;, prostaglandin D&lt;sub&gt;2&lt;/sub&gt;.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Previous studies demonstrated the heterogeneity of the nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) phenotype. Patients with severe asthma and aspirin hypersensitivity may exhibit differences in sputum mRNA gene expression. The aim of the study was to identify distinct transcriptional subtypes of severe asthma with aspirin hypersensitivity using unsupervised cluster analysis.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Sputum induction was performed in 27 patients with severe asthma and aspirin hypersensitivity who met 2022 Global Initiative for Asthma criteria for type 2 (T2) severe asthma. Using the transcriptional signatures of 87 genes, along with clinical characteristics and biomarker measurements, 2 distinct subtypes were identified and compared between study participants.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Two clusters were identified: cluster 1 (&lt;i&gt;n&lt;/i&gt; = 10) and cluster 2 (&lt;i&gt;n&lt;/i&gt; = 17). In cluster 1, low &lt;i&gt;GATA3&lt;/i&gt; expression was observed, along with several activated inflammatory genes, while cluster 2 was characterised by high &lt;i&gt;GATA3&lt;/i&gt; expression. Cluster 1 was characterised by increased sputum eosinophil count (&lt;i&gt;p&lt;/i&gt; = 0.04) and percentage (&lt;i&gt;p&lt;/i&gt; = 0.035), and decreased sputum macrophage count (&lt;i&gt;p&lt;/i&gt; = 0.003) and percentage (&lt;i&gt;p&lt;/i&gt; = 0.003). Patients in cluster 1 had increased sputum supernatant prostaglandin D&lt;sub&gt;2&lt;/sub&gt; levels (&lt;i&gt;p&lt;/i&gt; = 0.031). Patients in cluster 1 tended to have a higher Lund-Mackay score (&lt;i&gt;p&lt;/i&gt; = 0.074) and elevated peripheral blood eosinophilia (&lt;i&gt;p&lt;/i&gt; = 0.059).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Patients in cluster 1 exhibited T2 inflammation with low &lt;i&gt;GATA3&lt;/i&gt; expression, while those in cluster 2 showed T2 inflammation with high &lt;i&gt;GATA3&lt;/i&gt; expression. Sputum &lt;i&gt;GATA3&lt;/i&gt; expression may serve as a useful biomarker for differentiating distinct severe asthma subtypes in patients with N-ERD.&lt;/p&gt;</content:encoded>
         <dc:creator>
Radosław Kacorzyk, 
Piotr Szatkowski, 
Bogdan Jakieła, 
Adam Ćmiel, 
Marek Sanak, 
Lucyna Mastalerz
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Two Distinct Transcriptional Subtypes of Severe Type 2 Asthma in NSAID‐Exacerbated Respiratory Disease</dc:title>
         <dc:identifier>10.1111/cea.70253</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70253</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70253?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70254?af=R</link>
         <pubDate>Tue, 17 Feb 2026 00:58:49 -0800</pubDate>
         <dc:date>2026-02-17T12:58:49-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70254</guid>
         <title>Beyond Algorithms: Clinical Judgement in the Management of Allergic Rhinitis</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Gabriele Di Lorenzo, 
Marcello Melluso, 
Aurelio Seidita
</dc:creator>
         <category>EDITORIAL</category>
         <dc:title>Beyond Algorithms: Clinical Judgement in the Management of Allergic Rhinitis</dc:title>
         <dc:identifier>10.1111/cea.70254</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70254</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70254?af=R</prism:url>
         <prism:section>EDITORIAL</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70258?af=R</link>
         <pubDate>Tue, 17 Feb 2026 00:57:59 -0800</pubDate>
         <dc:date>2026-02-17T12:57:59-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70258</guid>
         <title>Serum Levels and Genetic Variants of CC16: Associations With Asthma and Lung Function Development</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Hans Jacob L. Koefoed, 
Yidan Sun, 
Ilse Hugtenburg, 
Stefano Guerra, 
Ulrike Gehring, 
Roel Vermeulen, 
Judith M. Vonk, 
Gerard H. Koppelman
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Serum Levels and Genetic Variants of CC16: Associations With Asthma and Lung Function Development</dc:title>
         <dc:identifier>10.1111/cea.70258</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70258</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70258?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70256?af=R</link>
         <pubDate>Mon, 16 Feb 2026 20:23:21 -0800</pubDate>
         <dc:date>2026-02-16T08:23:21-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70256</guid>
         <title>Letter to the Editor Regarding ‘National and Regional Drug Survival of Omalizumab in Chronic Spontaneous Urticaria: A Danish Cohort Study’</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Joaquín Borrás‐Blasco, 
Alejandro Valcuende‐Rosique, 
Silvia Cornejo‐Uixeda
</dc:creator>
         <category>CORRESPONDENCE</category>
         <dc:title>Letter to the Editor Regarding ‘National and Regional Drug Survival of Omalizumab in Chronic Spontaneous Urticaria: A Danish Cohort Study’</dc:title>
         <dc:identifier>10.1111/cea.70256</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70256</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70256?af=R</prism:url>
         <prism:section>CORRESPONDENCE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70255?af=R</link>
         <pubDate>Mon, 16 Feb 2026 00:00:00 -0800</pubDate>
         <dc:date>2026-02-16T12:00:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70255</guid>
         <title>House Dust Mite Sensitisation Effectively Differentiates Atopy From Non‐Atopy in the Tropical Environment of Southeast Asia</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Yang Yie Sio, 
Tan Ching Ong, 
Yee‐How Say, 
Kavita Reginald, 
Fook Tim Chew
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>House Dust Mite Sensitisation Effectively Differentiates Atopy From Non‐Atopy in the Tropical Environment of Southeast Asia</dc:title>
         <dc:identifier>10.1111/cea.70255</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70255</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70255?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70247?af=R</link>
         <pubDate>Mon, 16 Feb 2026 00:00:00 -0800</pubDate>
         <dc:date>2026-02-16T12:00:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70247</guid>
         <title>Optimal Treatment for Dysfunctional Breathing in Adults: An International Delphi Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
This international Delphi study identified five essential interventions for treating dysfunctional breathing, with assessment and home practice essential for delivery. The findings provide guidance for treatment options for both researchers and clinicians.

ABSTRACT

Background and Objectives
Dysfunctional breathing (DB) is common and impairs quality of life. Various non‐pharmacological interventions have been identified, but there is a lack of agreement regarding essential treatment components and delivery methods. This study aimed to gain consensus from experts and people with DB regarding the critical components, optimal format and delivery methods of non‐pharmacological DB interventions.


Methods
A two‐round Delphi process was conducted involving international experts, with each round followed by a consumer focus group. Online surveys were distributed using the Qualtrics platform. Components were defined as essential (median ≥ 4 on a 5‐point Likert scale, interquartile range [IQR] = 0), desirable (median = 5, IQR &gt; 0), or optional (median = 4, IQR &gt; 0). In the 2nd round, components with a median score ≤ 3 and IQR = 0 were eliminated, and components without consensus (IQR &gt; 0) were rescored.


Results
Participants in Round 1 included 46 experts and 5 focus group patients with DB, and in Round 2, 44 experts and 4 patients. Essential components for treating DB were a comprehensive assessment, breathing retraining with or without biofeedback, education, manual therapy, psychological therapy, and home practice of techniques. Desirable components were individualised home programs and information materials, and re‐assessment. Optional components were individualised modes of treatment delivery and exercise therapy.


Conclusion
This study identified five essential interventions for treating DB, with assessment and home practice essential for treatment delivery. Individualisation of interventions and treatment format is suggested. The findings provide a basis for the development of treatment options for people with DB.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/9da800ea-7aae-4a0d-a7ef-1b654474806b/cea70247-toc-0001-m.png"
     alt="Optimal Treatment for Dysfunctional Breathing in Adults: An International Delphi Study"/&gt;
&lt;p&gt;This international Delphi study identified five essential interventions for treating dysfunctional breathing, with assessment and home practice essential for delivery. The findings provide guidance for treatment options for both researchers and clinicians.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background and Objectives&lt;/h2&gt;
&lt;p&gt;Dysfunctional breathing (DB) is common and impairs quality of life. Various non-pharmacological interventions have been identified, but there is a lack of agreement regarding essential treatment components and delivery methods. This study aimed to gain consensus from experts and people with DB regarding the critical components, optimal format and delivery methods of non-pharmacological DB interventions.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A two-round Delphi process was conducted involving international experts, with each round followed by a consumer focus group. Online surveys were distributed using the Qualtrics platform. Components were defined as essential (median ≥ 4 on a 5-point Likert scale, interquartile range [IQR] = 0), desirable (median = 5, IQR &amp;gt; 0), or optional (median = 4, IQR &amp;gt; 0). In the 2nd round, components with a median score ≤ 3 and IQR = 0 were eliminated, and components without consensus (IQR &amp;gt; 0) were rescored.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Participants in Round 1 included 46 experts and 5 focus group patients with DB, and in Round 2, 44 experts and 4 patients. Essential components for treating DB were a comprehensive assessment, breathing retraining with or without biofeedback, education, manual therapy, psychological therapy, and home practice of techniques. Desirable components were individualised home programs and information materials, and re-assessment. Optional components were individualised modes of treatment delivery and exercise therapy.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study identified five essential interventions for treating DB, with assessment and home practice essential for treatment delivery. Individualisation of interventions and treatment format is suggested. The findings provide a basis for the development of treatment options for people with DB.&lt;/p&gt;</content:encoded>
         <dc:creator>
Janet Bondarenko, 
Jean Bremner, 
Brenda Button, 
Mark Hew, 
Anne E. Holland
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Optimal Treatment for Dysfunctional Breathing in Adults: An International Delphi Study</dc:title>
         <dc:identifier>10.1111/cea.70247</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70247</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70247?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70233?af=R</link>
         <pubDate>Fri, 13 Feb 2026 06:04:17 -0800</pubDate>
         <dc:date>2026-02-13T06:04:17-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70233</guid>
         <title>Comparative Efficacy of Biologicals for Chronic Rhinosinusitis With Nasal Polyps: A Systematic Review and Bayesian Network Meta‐Analysis</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Wenjing Chen, 
Yihao Shao, 
Stephen R. Durham, 
Martin Penagos, 
Mei Jiang, 
Mianquan Zhang, 
Xun Meng
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Comparative Efficacy of Biologicals for Chronic Rhinosinusitis With Nasal Polyps: A Systematic Review and Bayesian Network Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/cea.70233</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70233</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70233?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70246?af=R</link>
         <pubDate>Fri, 13 Feb 2026 00:00:00 -0800</pubDate>
         <dc:date>2026-02-13T12:00:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70246</guid>
         <title>Food Allergy in India: Delphi Consensus Statement by Indian Academy of Pediatrics (IAP)—Allergy and Applied Immunology Chapter</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
This graphical abstract summarises the Delphi consensus on food allergy in India, highlighting burden, common allergens, diagnostic approach, risk stratification, and management pathways. It emphasises early recognition, standardised diagnosis, prompt treatment of anaphylaxis, and the role of awareness, education, and consensus‐driven guidelines to improve outcomes in Indian children.

ABSTRACT
Food allergy is an emerging public health concern in India, driven by rapid urbanisation, changing dietary patterns, environmental influences, and increasing recognition of allergic diseases. Despite the growing burden, food allergy care in India is challenged by limited epidemiological data, variable diagnostic practices, and inadequate access to specialised services. These gaps underscore the need for standardised, context‐specific guidance tailored to the diverse sociocultural and dietary landscape of the country. This consensus document was developed by a multidisciplinary panel of allergy experts using a structured Delphi methodology to ensure methodological rigour and expert agreement. It provides a comprehensive overview of evidence‐based approaches to the diagnosis and management of food allergy, adapted to Indian clinical practice. The consensus recommends adoption of a standardised diagnostic framework incorporating detailed clinical history, skin prick testing, serum‐specific IgE estimation, and supervised oral food challenges, where appropriate. Recognition of region‐specific allergens—including milk, wheat, egg, peanut, fish, chickpea, lentils, and sesame—is emphasised to improve diagnostic accuracy and culturally relevant patient counselling. The document highlights the importance of comprehensive management strategies that integrate strict allergen avoidance with balanced, culturally appropriate nutritional planning and psychosocial support. Standardisation of clinical practice is advocated to reduce heterogeneity in care, facilitate early diagnosis, and improve patient outcomes. At a broader level, the consensus emphasises strengthening public health policies through clear food labelling, enhanced allergy education, and school‐based preparedness programs. Preventive strategies, including early supervised introduction of allergenic foods, are encouraged in appropriate settings. Advanced therapeutic options such as biologic agents and oral immunotherapy are recommended only for selected patients with severe disease and under specialist supervision. Finally, the consensus underscores the urgent need for robust epidemiological studies, improved diagnostic infrastructure, and enhanced professional training to address existing knowledge gaps. Collectively, these recommendations aim to improve quality of care, reduce disease burden, and support the development of effective, evidence‐based food allergy management in India.
</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/b8899a9f-3e9b-4ba6-a944-7b415c60a99e/cea70246-toc-0001-m.png"
     alt="Food Allergy in India: Delphi Consensus Statement by Indian Academy of Pediatrics (IAP)—Allergy and Applied Immunology Chapter"/&gt;
&lt;p&gt;This graphical abstract summarises the Delphi consensus on food allergy in India, highlighting burden, common allergens, diagnostic approach, risk stratification, and management pathways. It emphasises early recognition, standardised diagnosis, prompt treatment of anaphylaxis, and the role of awareness, education, and consensus-driven guidelines to improve outcomes in Indian children.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Food allergy is an emerging public health concern in India, driven by rapid urbanisation, changing dietary patterns, environmental influences, and increasing recognition of allergic diseases. Despite the growing burden, food allergy care in India is challenged by limited epidemiological data, variable diagnostic practices, and inadequate access to specialised services. These gaps underscore the need for standardised, context-specific guidance tailored to the diverse sociocultural and dietary landscape of the country. This consensus document was developed by a multidisciplinary panel of allergy experts using a structured Delphi methodology to ensure methodological rigour and expert agreement. It provides a comprehensive overview of evidence-based approaches to the diagnosis and management of food allergy, adapted to Indian clinical practice. The consensus recommends adoption of a standardised diagnostic framework incorporating detailed clinical history, skin prick testing, serum-specific IgE estimation, and supervised oral food challenges, where appropriate. Recognition of region-specific allergens—including milk, wheat, egg, peanut, fish, chickpea, lentils, and sesame—is emphasised to improve diagnostic accuracy and culturally relevant patient counselling. The document highlights the importance of comprehensive management strategies that integrate strict allergen avoidance with balanced, culturally appropriate nutritional planning and psychosocial support. Standardisation of clinical practice is advocated to reduce heterogeneity in care, facilitate early diagnosis, and improve patient outcomes. At a broader level, the consensus emphasises strengthening public health policies through clear food labelling, enhanced allergy education, and school-based preparedness programs. Preventive strategies, including early supervised introduction of allergenic foods, are encouraged in appropriate settings. Advanced therapeutic options such as biologic agents and oral immunotherapy are recommended only for selected patients with severe disease and under specialist supervision. Finally, the consensus underscores the urgent need for robust epidemiological studies, improved diagnostic infrastructure, and enhanced professional training to address existing knowledge gaps. Collectively, these recommendations aim to improve quality of care, reduce disease burden, and support the development of effective, evidence-based food allergy management in India.&lt;/p&gt;</content:encoded>
         <dc:creator>
Sowmya Arudi Nagarajan, 
Soundarya Mahalingam, 
Neeraj Gupta, 
Saibal Moitra, 
Dhanesh Volvoikar, 
Dipti Pujari, 
Gayatri S. Pandit, 
Jefferson Daniel, 
Kagithapu Surender, 
R. Krishna Mohan, 
P. A. Mahesh, 
Mitesh Kakkad, 
Mohit Poddar, 
Naresh Grover, 
Nayan Mani Deka, 
Rama Rajyam Datti, 
Sanjukta Dey, 
Sinchana Bhat, 
S. Narmada Ashok, 
Uppin Narayan Reddy, 
Vikram Patra, 
Vinay Mehta
</dc:creator>
         <category>CLINICAL PRACTICE GUIDELINE</category>
         <dc:title>Food Allergy in India: Delphi Consensus Statement by Indian Academy of Pediatrics (IAP)—Allergy and Applied Immunology Chapter</dc:title>
         <dc:identifier>10.1111/cea.70246</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70246</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70246?af=R</prism:url>
         <prism:section>CLINICAL PRACTICE GUIDELINE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70235?af=R</link>
         <pubDate>Thu, 12 Feb 2026 16:34:45 -0800</pubDate>
         <dc:date>2026-02-12T04:34:45-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70235</guid>
         <title>Prognostic Significance of Eosinophil Extracellular Traps in Chronic Rhinosinusitis and Innovative Nanosheets‐Based Clearance Therapy</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
EETs area emerges as a superior prognostic biomarker in ECRSwNP. EETs drive disease persistence via epithelial barrier disruption and immune dysregulation. TLPGA nanosheets effectively scavenge EETs and attenuate type 2 inflammation. EETs, eosinophil extracellular traps; FESS, functional endoscopic sinus surgery; PBMCs, peripheral blood mononuclear cells.

ABSTRACT

Background
Chronic rhinosinusitis with nasal polyps (CRSwNP) can be classified into Eosinophilic CRSwNP (ECRSwNP) and non‐Eosinophilic CRSwNP (nECRSwNP) based on eosinophilic infiltration in nasal polyps. However, no consensus criteria exist for eosinophilic infiltration in nasal polyps, including different cutoffs for eosinophil (EOS) counts or different EOS proportions among inflammatory cells.


Methods
Inferior turbinate (IT) tissues from controls (n = 27) and nasal polyp (NP) tissues from ECRSwNPs (n = 50) were collected. ECRSwNPs (n = 38) underwent 2‐year post‐FESS follow‐up. Clinical assessments (SNOT‐22, Lund‐Mackay, Lund‐Kennedy scores), eosinophil indicators (polyp/blood EOS counts, EETs area), and Th2 cytokines pre/post‐FESS were recorded for correlation analysis and prognostic model building. Subsequently, functional nanosheets TLPGA targeting EETs were synthesized and tested for EETs clearance in human EOS, epithelial cell models, and NP models.


Results
Our findings demonstrated positive correlations between EETs area and ECRSwNP severity, including Lund‐Mackay CT scores (r = 0.72, p &lt; 0.001), Lund‐Kennedy Endoscopic score (r = 0.57, p &lt; 0.001), IL‐4 (r = 0.50, p &lt; 0.001), IL‐5 (r = 0.50, p &lt; 0.001), IL‐13 (r = 0.39, p &lt; 0.01), and Periostin (r = 0.34, p &lt; 0.05). And we first demonstrated that increased preoperative EETs area predicts both impaired mucosal recovery and elevated nasal polyp uncontrolled risk within 2 years post‐FESS. Furthermore, we developed novel nanosheets TLPGA and demonstrated that TLPGA effectively scavenges EETs and alleviates the type 2 inflammatory cascade in human nasal polyp tissues and epithelial cell model.


Conclusion
These findings highlight the potential of EETs and EOS morphology in assessing preoperative ECRSwNP severity and predicting postoperative prognosis. Moreover, this also supports TLPGA as a promising therapeutic approach for managing ECRSwNP with high EETs levels.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/10315e7f-ed51-4679-90a2-49b68f3bda0e/cea70235-toc-0001-m.png"
     alt="Prognostic Significance of Eosinophil Extracellular Traps in Chronic Rhinosinusitis and Innovative Nanosheets-Based Clearance Therapy"/&gt;
&lt;p&gt;EETs area emerges as a superior prognostic biomarker in ECRSwNP. EETs drive disease persistence via epithelial barrier disruption and immune dysregulation. TLPG&lt;sub&gt;A&lt;/sub&gt; nanosheets effectively scavenge EETs and attenuate type 2 inflammation. EETs, eosinophil extracellular traps; FESS, functional endoscopic sinus surgery; PBMCs, peripheral blood mononuclear cells.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Chronic rhinosinusitis with nasal polyps (CRSwNP) can be classified into Eosinophilic CRSwNP (ECRSwNP) and non-Eosinophilic CRSwNP (nECRSwNP) based on eosinophilic infiltration in nasal polyps. However, no consensus criteria exist for eosinophilic infiltration in nasal polyps, including different cutoffs for eosinophil (EOS) counts or different EOS proportions among inflammatory cells.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Inferior turbinate (IT) tissues from controls (&lt;i&gt;n&lt;/i&gt; = 27) and nasal polyp (NP) tissues from ECRSwNPs (&lt;i&gt;n&lt;/i&gt; = 50) were collected. ECRSwNPs (&lt;i&gt;n&lt;/i&gt; = 38) underwent 2-year post-FESS follow-up. Clinical assessments (SNOT-22, Lund-Mackay, Lund-Kennedy scores), eosinophil indicators (polyp/blood EOS counts, EETs area), and Th2 cytokines pre/post-FESS were recorded for correlation analysis and prognostic model building. Subsequently, functional nanosheets TLPG&lt;sub&gt;A&lt;/sub&gt; targeting EETs were synthesized and tested for EETs clearance in human EOS, epithelial cell models, and NP models.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Our findings demonstrated positive correlations between EETs area and ECRSwNP severity, including Lund-Mackay CT scores (&lt;i&gt;r&lt;/i&gt; = 0.72, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), Lund-Kennedy Endoscopic score (&lt;i&gt;r&lt;/i&gt; = 0.57, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), IL-4 (&lt;i&gt;r&lt;/i&gt; = 0.50, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), IL-5 (&lt;i&gt;r&lt;/i&gt; = 0.50, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), IL-13 (&lt;i&gt;r&lt;/i&gt; = 0.39, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.01), and Periostin (&lt;i&gt;r&lt;/i&gt; = 0.34, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05). And we first demonstrated that increased preoperative EETs area predicts both impaired mucosal recovery and elevated nasal polyp uncontrolled risk within 2 years post-FESS. Furthermore, we developed novel nanosheets TLPG&lt;sub&gt;A&lt;/sub&gt; and demonstrated that TLPG&lt;sub&gt;A&lt;/sub&gt; effectively scavenges EETs and alleviates the type 2 inflammatory cascade in human nasal polyp tissues and epithelial cell model.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These findings highlight the potential of EETs and EOS morphology in assessing preoperative ECRSwNP severity and predicting postoperative prognosis. Moreover, this also supports TLPG&lt;sub&gt;A&lt;/sub&gt; as a promising therapeutic approach for managing ECRSwNP with high EETs levels.&lt;/p&gt;</content:encoded>
         <dc:creator>
Changhui Chen, 
Hang Li, 
Yilin Hou, 
Yihui Wen, 
Jian Li, 
Hua Zhong, 
Tong Lu, 
Zhengqi Li, 
Lin Sun, 
Shimin Lai, 
Yan Yan, 
Jieying Yan, 
Zihan Qiu, 
Nan Zhang, 
Claus Bachert, 
Zhaoxu Tu, 
Weiping Wen, 
Yi Wei
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Prognostic Significance of Eosinophil Extracellular Traps in Chronic Rhinosinusitis and Innovative Nanosheets‐Based Clearance Therapy</dc:title>
         <dc:identifier>10.1111/cea.70235</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70235</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70235?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70242?af=R</link>
         <pubDate>Thu, 12 Feb 2026 16:30:12 -0800</pubDate>
         <dc:date>2026-02-12T04:30:12-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70242</guid>
         <title>New Generation of Allergen Immunotherapy Using Virus‐Like Particles: A Comprehensive Review</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
ABSTRACT
Virus‐like particle (VLP)‐based allergen immunotherapy (AIT) represents a promising approach to treat allergic diseases by inducing specific IgG responses that suppress IgE‐mediated allergic reactions. VLPs, which are non‐infectious nanoparticles displaying antigens in repetitive arrays, efficiently activate B cells and antigen‐presenting cells, leading to robust polyclonal IgG production. These IgG antibodies can block allergen interactions with IgE receptors on mast cells and basophils, thereby preventing degranulation and allergic symptoms. Additionally, VLPs can stimulate innate immune pathways through Toll‐like receptor (TLR) signalling, promoting a Th1‐biased immune response that further contributes to the suppression of Th2‐driven allergic inflammation. VLP‐based allergy vaccines aim to re‐educate the immune system, promoting allergen tolerance, stimulating anti‐allergen antibody responses, and thereby disrupting pathogenic pathways. Preclinical studies have demonstrated that a few low‐dose administrations of VLPs conjugated with allergens can shift the typical Th2‐biased allergic response to a non‐pathogenic one. Clinical trials have shown that VLP‐based allergy vaccines are well‐tolerated and can elicit allergen‐specific IgG antibodies in humans. However, challenges remain in ensuring consistent quality control of VLP preparations, addressing pre‐existing immunity to VLP carriers and validating the efficacy of single‐allergen approaches for complex allergens. Future research should focus on optimising VLP formulations, exploring multivalent strategies and conducting large‐scale clinical trials to establish the safety and effectiveness of VLP‐based AIT.
</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Virus-like particle (VLP)-based allergen immunotherapy (AIT) represents a promising approach to treat allergic diseases by inducing specific IgG responses that suppress IgE-mediated allergic reactions. VLPs, which are non-infectious nanoparticles displaying antigens in repetitive arrays, efficiently activate B cells and antigen-presenting cells, leading to robust polyclonal IgG production. These IgG antibodies can block allergen interactions with IgE receptors on mast cells and basophils, thereby preventing degranulation and allergic symptoms. Additionally, VLPs can stimulate innate immune pathways through Toll-like receptor (TLR) signalling, promoting a Th1-biased immune response that further contributes to the suppression of Th2-driven allergic inflammation. VLP-based allergy vaccines aim to re-educate the immune system, promoting allergen tolerance, stimulating anti-allergen antibody responses, and thereby disrupting pathogenic pathways. Preclinical studies have demonstrated that a few low-dose administrations of VLPs conjugated with allergens can shift the typical Th2-biased allergic response to a non-pathogenic one. Clinical trials have shown that VLP-based allergy vaccines are well-tolerated and can elicit allergen-specific IgG antibodies in humans. However, challenges remain in ensuring consistent quality control of VLP preparations, addressing pre-existing immunity to VLP carriers and validating the efficacy of single-allergen approaches for complex allergens. Future research should focus on optimising VLP formulations, exploring multivalent strategies and conducting large-scale clinical trials to establish the safety and effectiveness of VLP-based AIT.&lt;/p&gt;</content:encoded>
         <dc:creator>
Alain Jacquet, 
Antonia Fettelschoss‐Gabriel, 
Pål Johansen
</dc:creator>
         <category>REVIEW ARTICLE</category>
         <dc:title>New Generation of Allergen Immunotherapy Using Virus‐Like Particles: A Comprehensive Review</dc:title>
         <dc:identifier>10.1111/cea.70242</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70242</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70242?af=R</prism:url>
         <prism:section>REVIEW ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70237?af=R</link>
         <pubDate>Thu, 12 Feb 2026 15:25:55 -0800</pubDate>
         <dc:date>2026-02-12T03:25:55-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70237</guid>
         <title>A Role for Non‐Canonical Caspases in Fungal Allergic Airway Disease</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Thomas J. Williams, 
Nazanin Zounemat Kermani, 
Luis E. Gonzales‐Huerta, 
Anand Shah, 
Ian M. Addcock, 
Kian Fan Chung, 
Darius Armstrong‐James, 
U‐BIORPED Study Group
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>A Role for Non‐Canonical Caspases in Fungal Allergic Airway Disease</dc:title>
         <dc:identifier>10.1111/cea.70237</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70237</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70237?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70234?af=R</link>
         <pubDate>Wed, 11 Feb 2026 19:11:50 -0800</pubDate>
         <dc:date>2026-02-11T07:11:50-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70234</guid>
         <title>AllergoOncology in Review: Harnessing Allergy in the Field of Oncology to Improve Patient Outcomes</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
ABSTRACT
The AllergoOncology field brings together the study of allergic and cancer immune responses, having evolved from early epidemiological studies that reported inverse associations between allergies, IgE and cancer risk. Insights from studying allergic inflammation are revealing previously unappreciated immune mechanisms that confer protective effects against cancer, and evasion pathways that facilitate tumour progression. AllergoOncology sheds light on cancers with poor prognosis, including glioma, where evidence has pointed to allergic triggers that may influence glioma biology through rewiring immune surveillance. Allergic signals point to new biomarkers that may identify groups at higher risk of developing cancer, aid patient stratification and help monitor treatment and clinical outcomes. Allergic mediators such as histamine and IgE levels are emerging biomarkers that can inform cancer risk and lead to clinical interventions that improve outcomes. Emerging cancer immunotherapies, such as tumour antigen‐specific IgEs, an evolving therapy class, are and will continue to be inspired by understanding allergic immune response mechanisms. Assays, including the Basophil Activation Test developed for monitoring and managing allergic reactions, are translated to the oncology clinic to evaluate hypersensitivity to anti‐cancer therapeutics. Allergy research brings fundamental benefits for oncology through understanding and harnessing allergic and cancer‐associated mechanisms in AllergoOncology for patient benefit.
</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;The AllergoOncology field brings together the study of allergic and cancer immune responses, having evolved from early epidemiological studies that reported inverse associations between allergies, IgE and cancer risk. Insights from studying allergic inflammation are revealing previously unappreciated immune mechanisms that confer protective effects against cancer, and evasion pathways that facilitate tumour progression. AllergoOncology sheds light on cancers with poor prognosis, including glioma, where evidence has pointed to allergic triggers that may influence glioma biology through rewiring immune surveillance. Allergic signals point to new biomarkers that may identify groups at higher risk of developing cancer, aid patient stratification and help monitor treatment and clinical outcomes. Allergic mediators such as histamine and IgE levels are emerging biomarkers that can inform cancer risk and lead to clinical interventions that improve outcomes. Emerging cancer immunotherapies, such as tumour antigen-specific IgEs, an evolving therapy class, are and will continue to be inspired by understanding allergic immune response mechanisms. Assays, including the Basophil Activation Test developed for monitoring and managing allergic reactions, are translated to the oncology clinic to evaluate hypersensitivity to anti-cancer therapeutics. Allergy research brings fundamental benefits for oncology through understanding and harnessing allergic and cancer-associated mechanisms in AllergoOncology for patient benefit.&lt;/p&gt;</content:encoded>
         <dc:creator>
Jakub Zydron, 
Anishaa Balaji, 
Jitesh Chauhan, 
Jack Alder, 
Xinyi Chen, 
Anna M. F. Wiegman, 
Aurelie Poli, 
Joanna Jacków‐Malinowska, 
Jack Cheeseman, 
Daniel I. R. Spencer, 
James McDonnell, 
James Spicer, 
Alexandra J. McCraw, 
Sophia N. Karagiannis
</dc:creator>
         <category>REVIEW ARTICLE</category>
         <dc:title>AllergoOncology in Review: Harnessing Allergy in the Field of Oncology to Improve Patient Outcomes</dc:title>
         <dc:identifier>10.1111/cea.70234</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70234</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70234?af=R</prism:url>
         <prism:section>REVIEW ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70244?af=R</link>
         <pubDate>Tue, 10 Feb 2026 16:33:59 -0800</pubDate>
         <dc:date>2026-02-10T04:33:59-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70244</guid>
         <title>Binational Association Between Asthma and Life's Essential 8 in South Korea and the United States: A Nationwide Representative Comparative Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Minwoo Jung, 
Taelim Choi, 
Jinyoung Jeong, 
Jeongseon Oh, 
Jaeyu Park, 
Seohyun Hong, 
Yoon Lee, 
Masoud Rahmati, 
Hanseul Cho, 
Yerin Hwang, 
Dong Keon Yon
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Binational Association Between Asthma and Life's Essential 8 in South Korea and the United States: A Nationwide Representative Comparative Study</dc:title>
         <dc:identifier>10.1111/cea.70244</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70244</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70244?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70238?af=R</link>
         <pubDate>Tue, 10 Feb 2026 16:25:06 -0800</pubDate>
         <dc:date>2026-02-10T04:25:06-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70238</guid>
         <title>Basophil Activation Test for the In Vitro Diagnosis of Tocilizumab Hypersensitivity</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Ana Koren, 
Luka Dejanović, 
Peter Korošec, 
Peter Kopač
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Basophil Activation Test for the In Vitro Diagnosis of Tocilizumab Hypersensitivity</dc:title>
         <dc:identifier>10.1111/cea.70238</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70238</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70238?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70239?af=R</link>
         <pubDate>Mon, 09 Feb 2026 01:14:46 -0800</pubDate>
         <dc:date>2026-02-09T01:14:46-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70239</guid>
         <title>Patients With Chronic Urticaria Have Higher Health‐Care Resource Utilisation: A Danish Nationwide Case–Control Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Jennifer Astrup Sørensen, 
Somaia Naassan, 
Christian Vestergaard, 
Nana Aviaaja Lippert Rosenø, 
Cæcilie Bachdal Johansen, 
Alexander Egeberg, 
Jacob P. Thyssen, 
Panagiotis Orfanos, 
Nadine Chapman‐Rothe, 
Tara Raftery, 
Simon Francis Thomsen, 
Zarqa Ali
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Patients With Chronic Urticaria Have Higher Health‐Care Resource Utilisation: A Danish Nationwide Case–Control Study</dc:title>
         <dc:identifier>10.1111/cea.70239</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70239</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70239?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70232?af=R</link>
         <pubDate>Sun, 08 Feb 2026 17:40:43 -0800</pubDate>
         <dc:date>2026-02-08T05:40:43-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70232</guid>
         <title>Pro‐Inflammatory Dietary Patterns Are Associated With Atopic but Not Non‐Atopic Dermatitis in Asian Adults: Evidence From a Cross‐Sectional Study</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Jun Jie Lim, 
Jia Yi Karen Wong, 
Zongxun Huang, 
Kavita Reginald, 
Yee‐How Say, 
Mei Hui Liu, 
Fook Tim Chew
</dc:creator>
         <category>RESEARCH LETTER</category>
         <dc:title>Pro‐Inflammatory Dietary Patterns Are Associated With Atopic but Not Non‐Atopic Dermatitis in Asian Adults: Evidence From a Cross‐Sectional Study</dc:title>
         <dc:identifier>10.1111/cea.70232</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70232</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70232?af=R</prism:url>
         <prism:section>RESEARCH LETTER</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/cea.70230?af=R</link>
         <pubDate>Sun, 08 Feb 2026 17:39:52 -0800</pubDate>
         <dc:date>2026-02-08T05:39:52-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/13652222?af=R">Wiley: Clinical &amp; Experimental Allergy: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/cea.70230</guid>
         <title>Identifying an At‐Risk Asthma Phenotype: Allergy and Recurrent Infections Predict Severe Disease</title>
         <description>Clinical &amp;amp;Experimental Allergy, EarlyView. </description>
         <dc:description>
Allergic asthma and recurrent antibiotic‐treated infections synergistically accelerate progression to severe asthma, underscoring the need for early, targeted preventive strategies.

ABSTRACT

Background
Asthma severity is influenced by complex immunologic and environmental factors. While allergic asthma is linked to increased susceptibility to respiratory infections, the combined role of allergy and antibiotic‐treated infections in progression to severe asthma has not been fully evaluated.


Objective
To evaluate whether allergic asthma and recurrent respiratory infections (RRI) requiring antibiotics are associated with increased risk of developing severe asthma.


Methods
We conducted a registry‐based cohort study using Swedish national registry data. Adults with mild‐to‐moderate asthma were identified in 2014 (baseline) based on prescription records and absence of severe disease indicators. During a two‐year exposure window (2015–2016), RRI was defined as ≥ 2 antibiotic prescriptions for lower respiratory tract infections. The outcome was development of severe asthma during 2017–2019, based on ERS/ATS treatment criteria. Allergic asthma was defined by ≥ 2 prescriptions for anti‐allergic medications at baseline.


Results
Among 113,393 patients, 24,692 (21.8%) had allergic asthma. RRI occurred more frequently in allergic versus non‐allergic asthma (7.5% vs. 5.9%, p &lt; 0.001). A total of 869 patients (0.77%) developed severe asthma. Incidence was higher in those with RRI and highest among patients with both allergic asthma and RRI (2.0%), corresponding to a relative risk of 3.47 (95% CI: 2.49–4.83) versus patients with neither exposure. Results were consistent after adjustment for age, sex and comorbidities.


Conclusion
Allergic asthma and antibiotic‐treated respiratory infections were independent and additive predictors of severe asthma progression. These findings support a clinically actionable risk profile and may inform targeted preventive strategies in asthma management.

</dc:description>
         <content:encoded>&lt;img src="https://onlinelibrary.wiley.com/cms/asset/cb2ba0f0-e2e4-4a3c-a218-140cab08b6e7/cea70230-toc-0001-m.png"
     alt="Identifying an At-Risk Asthma Phenotype: Allergy and Recurrent Infections Predict Severe Disease"/&gt;
&lt;p&gt;Allergic asthma and recurrent antibiotic-treated infections synergistically accelerate progression to severe asthma, underscoring the need for early, targeted preventive strategies.&lt;/p&gt;
&lt;br/&gt;
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Asthma severity is influenced by complex immunologic and environmental factors. While allergic asthma is linked to increased susceptibility to respiratory infections, the combined role of allergy and antibiotic-treated infections in progression to severe asthma has not been fully evaluated.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To evaluate whether allergic asthma and recurrent respiratory infections (RRI) requiring antibiotics are associated with increased risk of developing severe asthma.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;We conducted a registry-based cohort study using Swedish national registry data. Adults with mild-to-moderate asthma were identified in 2014 (baseline) based on prescription records and absence of severe disease indicators. During a two-year exposure window (2015–2016), RRI was defined as ≥ 2 antibiotic prescriptions for lower respiratory tract infections. The outcome was development of severe asthma during 2017–2019, based on ERS/ATS treatment criteria. Allergic asthma was defined by ≥ 2 prescriptions for anti-allergic medications at baseline.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Among 113,393 patients, 24,692 (21.8%) had allergic asthma. RRI occurred more frequently in allergic versus non-allergic asthma (7.5% vs. 5.9%, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). A total of 869 patients (0.77%) developed severe asthma. Incidence was higher in those with RRI and highest among patients with both allergic asthma and RRI (2.0%), corresponding to a relative risk of 3.47 (95% CI: 2.49–4.83) versus patients with neither exposure. Results were consistent after adjustment for age, sex and comorbidities.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Allergic asthma and antibiotic-treated respiratory infections were independent and additive predictors of severe asthma progression. These findings support a clinically actionable risk profile and may inform targeted preventive strategies in asthma management.&lt;/p&gt;</content:encoded>
         <dc:creator>
Emilie Johanning Bari, 
Susanne Hansen, 
Patrik Sandin, 
Olivia Ernstsson, 
Kirk Geale, 
Apostolos Bossios, 
Lauri Lehtimäki, 
Christer Janson, 
Charlotte Ulrik, 
Hannu Kankaanranta, 
Bernt Bøgvald Aarli, 
Anna Von Bülow, 
Arja Viinanen, 
Asger Sverrild, 
Dóra Lúdvíksdóttir, 
Helena Backman, 
Johannes Martin Schmid, 
Jussi Karjalainen, 
Leif Bjermer, 
Maritta Kilpeläinen, 
Ole Hilberg, 
Paula Kauppi, 
Sverre Lehmann, 
Thomas Sandström, 
Tina Skjold, 
Unnur Steina Björnsdóttir, 
Valentyna Yasinska, 
Vibeke Backer, 
Alan Altraja, 
Celeste Porsbjerg
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Identifying an At‐Risk Asthma Phenotype: Allergy and Recurrent Infections Predict Severe Disease</dc:title>
         <dc:identifier>10.1111/cea.70230</dc:identifier>
         <prism:publicationName>Clinical &amp; Experimental Allergy</prism:publicationName>
         <prism:doi>10.1111/cea.70230</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/cea.70230?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
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