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        <title>Frontiers in Allergy | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/allergy</link>
        <description>RSS Feed for Frontiers in Allergy | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-16T21:48:30.145+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1789143</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1789143</link>
        <title><![CDATA[The AhR–TLR4 axis in non-IgE-mediated Cow's milk allergy: a systematic review with integrated multi-omics corroboration]]></title>
        <pubdate>2026-04-14T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Wei Kong</author><author>Bin Wu</author><author>Ying Huang</author><author>Haiying Liu</author><author>Congfu Huang</author>
        <description><![CDATA[Background & aimsNon-IgE-mediated cow's milk allergy (non-IgE-CMPA) is the most prevalent form of CMPA in infancy; however, its pathogenesis is still poorly understood, which impedes the development of targeted nutritional strategies. Recent evidence suggests a connection between gut dysbiosis and immune dysregulation. Therefore, this systematic review, incorporating multi-omics corroboration, sought to clarify a pathogenic axis driven by dysbiosis and involving the aryl hydrocarbon receptor (AhR) and Toll-like receptor 4 (TLR4). Furthermore, the review aimed to evaluate related predictive biomarkers and potential therapeutic approaches.MethodsWe synthesized evidence from 39 studies of infants (0–3 years) with physician-confirmed non-IgE-CMPA, following PRISMA guidelines. To visually corroborate key mechanistic pathways at cellular resolution, we performed an integrative analysis of publicly available single-cell RNA sequencing datasets from pediatric intestinal biopsies.ResultsNon-IgE-mediated CMPA exhibits a distinct gut dysbiosis signature, characterized by decreased Bifidobacterium and increased Enterobacteriacea. This dysbiosis is associated with reduced microbial AhR ligands and TLR4 pathway in intestinal epithelial cells. A B/E ratio <0.5 at 3 months of age predicted persistent allergy (HR = 1.9, AUC = 0.82). scRNA-seq data confirmed IEC-specific upregulation of TLR4 co-receptors (CD14, LY96), activation of the NLRP3 inflammasome, and reduced expression of intestinal barrier integrity markers. Synbiotic intervention (LGG + HMOs) was associated with a 67% resolution of symptoms.ConclusionEarly-life gut dysbiosis may disrupt AhR–TLR4 crosstalk, leading to NLRP3-mediated inflammation and barrier dysfunction in non-IgE-mediated CMPA. Bradford Hill criteria suggest a causal relationship for this pathway. Furthermore, the B/E ratio holds promise for early risk stratification, and synbiotics represent a potential mechanism-guided nutritional strategy for restoring microbial-immune homeostasis.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/view/CRD42025104533, PROSPERO CRD420251045333.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1760856</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1760856</link>
        <title><![CDATA[Digital health in allergy care: current practices, evidence, and future prospects]]></title>
        <pubdate>2026-04-14T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Olga Lourenço</author><author>Adriano N. Raposo</author>
        <description><![CDATA[This mini-review summarizes the current applications of digital tools in allergy care, including telemedicine platforms, mobile health technologies, and AI-based decision support systems. It critically examines available evidence, benefits, and challenges for clinical practice and outlines future directions for integrating digital health into personalized allergy management. Mobile apps and wearable sensors enable real-time tracking of symptoms, medication use, and environmental triggers, providing actionable data that supports proactive disease management. Continuous data streams enhance clinicians’ ability to adjust treatment promptly and personalize care. AI-driven tools offer emerging opportunities for predictive modeling and decision support, while telemedicine expands access and convenience. Together, these innovations may support more patient-centered, equitable, and data-informed care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1783914</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1783914</link>
        <title><![CDATA[Hereditary α-tryptasemia; a review of mechanisms linking α-tryptase gene dosage to intestinal homeostasis and immunopathology]]></title>
        <pubdate>2026-04-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Ilaria M. Simeone</author><author>Michelle Galeas-Pena</author><author>Katelyn White</author><author>Brandy Sullivan</author><author>Alexandra Morelli</author><author>Jocelyn A. Silvester</author><author>Liza Konnikova</author><author>Amelie Therrien</author><author>Sarah C. Glover</author>
        <description><![CDATA[Hereditary α-tryptasemia (HαT) is a genetic trait characterized by increased TPSAB1 copy number. Identified in 2015, the HαT trait impacts approximately 4%–6% of individuals of European ancestry and manifests with core clinical features in one-third of individuals who test positive for the genetic trait. HαT represents a natural human model of α-tryptase overexpression which can be leveraged to better and more comprehensively understand tryptase and mast cell (MC) biology at the tissue level. In this review, we synthesize emerging evidence demonstrating that HαT is a clinically significant modifier of disease in the gastrointestinal (GI) tract. We summarize findings demonstrating that HαT impacts small intestinal immunopathology even in the absence of overt GI pathology. In celiac disease, coexisting HαT is associated with increased duodenal MCs and persistent GI symptoms (diarrhea, bloating, abdominal pain) despite a gluten-free diet. We also review emerging data indicating that HαT may act as a disease modifier in inflammatory bowel disease (IBD); increased α-tryptase gene dosage is associated with intestinal MC activation and increased expression of MRGPRX2. These changes may amplify MC–mediated inflammatory pathways within the intestinal mucosa and contribute to the complexity of immune signaling traditionally attributed to T-cell–driven inflammation in IBD. Taken together, emerging modern cellular and molecular biology evidence suggests that the natural overexpression of α-tryptase in HαT alters MC behavior and GI intestinal immunopathology, thereby modifying disease outcomes across a spectrum of GI illnesses.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1772380</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1772380</link>
        <title><![CDATA[Asthma and corticosteroids “odi et amo”: how to deal with it?]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Luca Borsari</author><author>Laura Carbonieri</author><author>Luca M. Verdini</author><author>Valentina Ruggieri</author><author>Bianca Beghe’</author>
        <description><![CDATA[Asthma is a chronic, heterogeneous respiratory disease that affects more than 300 million individuals worldwide and is responsible for substantial morbidity, mortality and healthcare burden. Chronic airway inflammation plays a central role in symptom expression, disease progression, and response to therapy. Corticosteroids, both inhaled and systemic, are the cornerstone of asthma treatment. However, it is well known that the use and abuse of systemic corticosteroids is almost invariably associated to the development of significant acute and chronic adverse events. Epidemiological data report that despite the availability of new target therapy, e.g., biologics, in real practice systemic steroids are still overused, and in this review, we highlight strategies 1) to identify and screen patients at risk of developing corticosteroids adverse events and 2) to reduce them.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1840104</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1840104</link>
        <title><![CDATA[Editorial: Biologics for airway diseases: from bench to bedside]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Andreas M. Matthaiou</author><author>Nikoleta Bizymi</author><author>Dina Visca</author><author>Lena Uller</author><author>Nikolaos G. Papadopoulos</author><author>Alexander G. Mathioudakis</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1806555</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1806555</link>
        <title><![CDATA[The relationship between allergic rhinitis and sleep disorders and mental health]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xiaoning Feng</author><author>Zhaowei Gu</author><author>Yunxiu Wang</author>
        <description><![CDATA[Allergic Rhinitis (AR) is a highly prevalent IgE-mediated chronic inflammatory disease of the nasal mucosa worldwide. Its incidence is continuously increasing and has become one of the important chronic diseases affecting public health. Recent studies have gradually revealed that AR not only presents with local symptoms such as nasal congestion, runny nose, sneezing, and nasal itching, but is also closely related to a wide range of physical and mental health problems, especially mental and psychological disorders (such as anxiety and depression) and decreased sleep quality. There is a complex two-way or even circular interaction between these three factors. This article systematically reviews the epidemiological characteristics and pathophysiological mechanisms of AR, and focuses on exploring the association pathways and potential mechanisms between AR and mental health as well as sleep disorders, including neuroimmune regulation (such as inflammatory mediators, HPA axis function), psychological and behavioral factors, and social function impairment. Based on this, the article further summarizes the assessment tools and multimodal intervention strategies for mental and psychological problems and sleep disorders in AR patients, covering drug treatment, psychotherapy, sleep hygiene education, and comprehensive health management, etc. This article integrates current evidence and provides a theoretical framework for a comprehensive understanding of the multi-dimensional impact of AR, and offers references for comprehensive assessment and individualized intervention in clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1816013</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1816013</link>
        <title><![CDATA[Two combinations of house dust mite allergens show similar performance than extracts for asthma diagnosis]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Victoria Marrugo</author><author>Josefina Zakzuk</author><author>Randy Reina</author><author>Karen Donado</author><author>Ronald Regino</author><author>Isabel Gil</author><author>Caterine Meza</author><author>Dilia Mercado</author><author>Enrique Fernández-Caldas</author><author>Leonardo Puerta</author><author>Nathalie Acevedo</author><author>Luis Caraballo</author>
        <description><![CDATA[IntroductionMolecular allergy diagnostics for house dust mite (HDM) sensitization includes both allergenic molecules and extracts, but extracts have batch-to-batch variability, incomplete allergen representation and cross-reactivity, which confound results and reduces test accuracy. However, although using extract-free arrays could solve these problems, there is no study that formally supports this change. Therefore, the aim of this study was to compare the diagnostic performance and clinical relevance of measuring specific IgE to Dermatophagoides pteronyssinus and Blomia tropicalis extracts vs. two allergen combinations, Blo t 2/Blo t 5/Blo t 21 and Der p 1/Der p 2/Der p 23.MethodsIn 201 adults with asthma and matched controls, diagnostic performance of specific IgE towards molecular allergen combinations and extracts were compared using receiver operator characteristics analysis, with physician-diagnosed asthma as reference standard. Associations between specific IgE (extracts and combinations) and type 2 inflammation biomarkers (fractional exhaled nitric oxide and blood eosinophils) were also evaluated.ResultsSpecific IgE frequencies and levels were higher in patients. Allergen combinations and extracts showed equivalent performance. The area under the curve of the combination Blo t 2/Blo t 5/Blo t 21 was similar to that of the B. tropicalis extract: 0.783 and 0.808 respectively (p = 0.42). Likewise, the area under the curve of the combination Der p 1/Der p 2/Der p 23 was 0.793 and that of extract was 0.788 (p = 0.8). Notably, IgE response to D. pteronyssinus allergens was more specific than the extract and significantly associated with fractional exhaled nitric oxide and blood eosinophils.ConclusionOur findings provide, for the first time, direct evidence that specific allergen combinations have similar diagnostic performance to HDM extracts in molecular diagnostics, improving test accuracy and supporting a shift toward standardized, molecular-resolved diagnostic strategies. In addition, we found that allergen combinations, and not HDM extracts, are strongly associated with type 2 inflammation biomarkers, supporting their use for personalized asthma management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1817101</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1817101</link>
        <title><![CDATA[Emerging molecular and environmental biomarkers of shrimp allergy in African Americans in the US]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Tanmoy Mondal</author><author>Dalyngs Duvelsaint</author><author>Kingston Griffin</author><author>McKenzie Williams</author><author>Oluwaseyitodun Johnson</author><author>Zara Campbell</author><author>Carla M. Davis</author>
        <description><![CDATA[Shrimp allergy (SA), a major cause of food-induced anaphylaxis, represents a disproportionate and under-characterized burden among African American (AA) populations in the United States. Unlike many childhood food allergies, SA is often persistent and commonly presents in adolescence or adulthood, suggesting a role for cumulative environmental exposures in disrupting oral tolerance. A key diagnostic challenge in AA communities is the high prevalence of IgE sensitization to shrimp tropomyosin (Pen a 1), which shares strong structural homology with cockroach and house dust mite tropomyosins, leading to frequent cross-reactive but clinically irrelevant sensitization in urban settings. This review critically examines molecular and environmental biomarkers of SA with a focus on AA populations. We assess the limitations of extract-based IgE testing and component-resolved diagnostics, highlighting how single-component assays may overestimate true clinical allergy. We emphasize the added value of functional assays, particularly the basophil activation test, in distinguishing sensitization from challenge-confirmed allergies. Mechanistically, we discuss how chronic exposure to indoor arthropod allergens, air pollution, and socioenvironmental stressors may drive epithelial barrier dysfunction, IL-33 release, and amplification of type 2 immune pathways, lowering reaction thresholds and influencing disease persistence. We identify key gaps, including limited oral food challenge–confirmed data and underrepresentation of AA cohorts. Finally, we propose equity-centered, integrative research frameworks combining molecular diagnostics, functional assays, environmental assessment, and multi-omics to improve diagnostic precision and advance clinical equity in SA care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1784032</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1784032</link>
        <title><![CDATA[Toward personalized prediction: a multicenter machine learning model for omalizumab response duration in moderate-to-severe perennial allergic rhinitis]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ziqi Miao</author><author>Lin Dong</author><author>Jin Liu</author><author>Le Li</author><author>Xiang Dong</author><author>Shuchen Zhang</author><author>Rongfei Zhu</author><author>Yuqin Deng</author>
        <description><![CDATA[BackgroundOmalizumab effectively improves quality of life in patients with moderate-to-severe perennial allergic rhinitis (PAR) uncontrolled by conventional medications. However, the duration of its efficacy remains unclear, and there is a lack of effective tools for individualized prediction.ObjectiveThis study aimed to identify predictors of Omalizumab duration of efficacy in moderate-to-severe PAR patients, then develop and validate an interpretable, machine learning-based predictive model to forecast the duration of efficacy following treatment.MethodsThis multicenter retrospective study included 561 patients with moderate-to-severe PAR treated with Omalizumab at three clinical institutions. The trial was registered at Chinese Clinical Trial Registry, ChiCTR2500112034. Patient characteristics included age, sex, serum total IgE concentration, serum specific IgE (sIgE) concentrations including Dermatophagoides pteronyssinus (D1) and Dermatophagoides farina (D2), comorbid conditions (asthma, urticaria, conjunctivitis, atopic dermatitis), and injection frequency. Univariate and multivariate Cox regression were employed to investigate independent predictors of Omalizumab efficacy, with restricted cubic splines for dose-response analysis. Five survival machine learning models (CPH, XGBoost, RSF, SSVM, CoxBoost) were constructed and compared by comprehensive metrics. The optimal model was interpreted using the SHapley Additive exPlanations (SHAP) and deployed as an online web application.ResultsUnivariate Cox regression identified age, D1, D2, asthma and injection frequency as independent factors affecting Omalizumab efficacy duration. Multivariate analysis did not confirm D2 as significant. Dose-response analysis demonstrated enhanced protective effects beyond four injections. Among the five models, RSF demonstrated robust predictive performance. SHAP analysis identified injection frequency, age, D1, D2, and coexisting asthma as the most critical factors.ConclusionThis study developed and validated a machine learning-based model capable of forecasting the duration of Omalizumab efficacy in moderate-to-severe PAR based on readily available clinical variables.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1667661</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1667661</link>
        <title><![CDATA[One-session asthma curriculum for all K–8th grade students: impact on knowledge, attitudes, and self-efficacy]]></title>
        <pubdate>2026-04-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Caroline Luff</author><author>Alexandra Knitter</author><author>Bolanle Ogbara</author><author>LaToya Gregory</author><author>Monica Kowalczyk</author><author>Anna Volerman</author>
        <description><![CDATA[BackgroundSchools are critical places to support children with asthma. Few school-based interventions focus on classmates without asthma, who can influence peers’ asthma self-management.ObjectiveTo describe a one-session asthma curriculum for all Kindergarten-8th grade students and evaluate impact on knowledge, attitudes, and self-efficacy.MethodsIn collaboration with three Chicago schools, we adapted and implemented a one-session asthma curriculum for K-8th grades. Students completed a post-session survey to assess asthma knowledge, attitudes, and self-efficacy. Pearson's Chi-squared tests analyzed differences between grades and student-reported asthma diagnosis.ResultsIn total, 603 students participated in a session, of which 485 completed the survey; 19% reported having asthma. Most students correctly answered knowledge questions on pathophysiology (82%), transmission (79%), symptoms (65%), triggers (65%), medication use (90%), and episode management (51%). More older students understood pathophysiology (85% vs. 72%, p = 0.002), medication use (93% vs. 83%, p = 0.002), and episode management (55% vs. 31%, p < 0.001), vs. younger students. Of all students, 83% indicated positive attitudes about asthma care and 49% about physical activity participation, with differences based on grade (asthma care: older 86% vs. younger 74%, p = 0.002) and diagnosis (physical activity participation: asthma 63% vs. no asthma 45%, p = 0.002). Most students indicated positive self-efficacy to help classmates with asthma episodes (74%), with more younger students doing so than older students (83% vs. 71%, p = 0.01).ConclusionStudents had high asthma knowledge and self-efficacy after a one-session all-student asthma curriculum; attitudes were mixed. School-based asthma education is feasible and has positive outcomes for all K–8th grade students.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1789783</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1789783</link>
        <title><![CDATA[Impact of sputum neutrophilia on the efficacy of biologics in severe asthma]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Patrizia Pignatti</author><author>Martina Zappa</author><author>Francesco Ardesi</author><author>Marco Vanetti</author><author>Rosella Centis</author><author>Antonio Spanevello</author><author>Dina Visca</author>
        <description><![CDATA[IntroductionPatients with severe asthma have new therapeutic opportunities with biologic agents, reducing exacerbation rates, symptom scores, and oral corticosteroid use; however, their effects on lung function appear to be variable. The aim of this study is to evaluate the clinical and inflammatory outcomes of biologic therapy in patients with severe asthma, stratified according to baseline bronchial inflammation.MethodsThis was a retrospective observational study in patients with severe asthma at 6 and 12 months after initiation of biologic therapy. Patients were categorized according to their baseline airway inflammatory profile. The inflammatory biomarkers evaluated included induced sputum, fractional exhaled nitric oxide (FeNO), and peripheral blood leukocyte counts. Lung function, comorbidities, exacerbation rate, and asthma control (assessed by ACQ-6 and ACT) were also recorded.ResultsA total of 113 patients with severe asthma were analyzed. Patients with a paucigranulocytic pattern were excluded from further analyses due to their small number (n = 10). Among the remaining subjects (n = 103), 62.8% exhibited an eosinophilic pattern, 13.3% a mixed granulocytic pattern, and 15.0% a neutrophilic pattern. Most neutrophilic patients (82.7%) presented elevated type 2 (T2) biomarkers (FeNO and/or blood eosinophils). Differences in baseline biomarkers and comorbidities reflected the underlying airway inflammatory patterns; forced vital capacity (FVC, L) was lower in neutrophilic patients compared with the other groups. Neutrophilic patients had higher frequencies of obstructive sleep apnea and lower chronic rhinosinusitis with nasal polyps than eosinophilic subjects. During follow-up, all patients showed a significant reduction in their ability to produce sputum (p < 0.001), as well as significant decreases in exacerbation rate and symptom burden. Eosinophilic and mixed granulocytic patients exhibited significant improvements in lung function, whereas neutrophilic patients did not. Only eosinophilic patients showed a significant reduction in airway inflammation. Oral corticosteroid doses decreased across all groups, but significantly only in eosinophilic patients. Clinical and inflammatory improvements were observed after 6 months of biologic therapy, with no further significant changes at 12 months.ConclusionsAfter 12 months of biologic therapy, patients showed phenotype-dependent responses, with neutrophilic patients demonstrating smaller clinical and inflammatory improvements compared with those with eosinophilic or mixed granulocytic phenotypes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1777688</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1777688</link>
        <title><![CDATA[Women hormones and hypersensitivity: allergic diseases in menopause]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Elitsa Valerieva</author><author>Mariela Vasileva</author><author>Krasimira Baynova</author><author>Borislava Krusheva</author><author>Elena Petkova</author><author>Miroslava Nenova</author><author>Plamena Novakova</author><author>Maria Staevska</author><author>Stefan Cimbollek</author><author>Anna Valerieva</author>
        <description><![CDATA[Menopause is a midlife endocrinological transition that profoundly affects immune regulation, vascular function, and tissue homeostasis, influencing the onset, severity, and clinical expression of allergic diseases. Declining and fluctuating estrogen and progesterone levels modulate mast-cell activity, T2 inflammation, and vascular permeability, contributing to distinct phenotypes in asthma, allergic rhinitis, chronic cough, skin allergies, drug hypersensitivity, anaphylaxis, and angioedema. Clinical observations suggest menopause may exacerbate existing conditions or trigger new-onset disease, with hormone replacement therapy (HRT) potentially modifying disease trajectories. Obesity, comorbidities, polypharmacy, and age-related physiological changes further shape symptom patterns and therapeutic responses. Despite increasing recognition of these effects, mechanistic understanding remains limited, and evidence-based guidelines for diagnosis, management, and individualized therapy in peri- and postmenopausal women are scarce. This review synthesizes current knowledge on hormonal influences in allergic diseases, highlights menopause-specific clinical considerations, and identifies major research gaps. Understanding the interplay between sex hormones, immune function, and allergic disease expression is critical for optimizing care. Clinicians should integrate peri-/menopause status into assessment and management, and future research should aim to clarify pathophysiologic mechanisms, risk factors, and tailored interventions for women in midlife.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1830021</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1830021</link>
        <title><![CDATA[Editorial: Allergies in focus, tales from the less explored world: prevalence, allergens, and treatment strategies in Latin America and Africa]]></title>
        <pubdate>2026-04-07T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Renata Curciarello</author><author>Cecilia I. Muglia</author><author>Paola L. Smaldini</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1823731</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1823731</link>
        <title><![CDATA[Editorial: Clinical and molecular aspects of managing chronic urticaria: identifying endotypes, phenotypes, and factors determining responses and resistance to treatment]]></title>
        <pubdate>2026-04-07T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Andac Salman</author><author>Indrashis Podder</author><author>Jonny Peter</author><author>Ana Maria Gimenez-Arnau</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1842963</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1842963</link>
        <title><![CDATA[Retraction: Mechanisms for Alternaria alternata function in the skin during induction of peanut allergy in neonatal mice with skin barrier mutations]]></title>
        <pubdate>2026-04-02T00:00:00Z</pubdate>
        <category>Retraction</category>
        
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1761840</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1761840</link>
        <title><![CDATA[Gut microbiome modulation in allergic rhinitis: from current evidence to emerging therapies]]></title>
        <pubdate>2026-04-01T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Siu-Jung Au Yong</author><author>Amanda Sandra Lestari Lee</author><author>Vetriselvan Subramaniyan</author><author>Chiau Ming Long</author><author>Salina Husain</author><author>Kavita Reginald</author><author>Hooi-Leng Ser</author>
        <description><![CDATA[Allergic rhinitis (AR) is a common inflammatory disorder of the upper airway that is primarily managed with pharmacotherapy, biologics and allergen immunotherapy. However, a substantial proportion of patients experience incomplete or insufficient symptom control, treatment-related adverse effects, or poor adherence. Increasing evidence has linked AR with alterations in microbial composition across multiple mucosal sites, including the gut, highlighting potential roles for host-microbiome interactions in the regulation of allergic inflammation, although causal relationships remain incompletely defined. This narrative mini-review synthesizes current evidence on gut microbiome-based interventions for allergic rhinitis (AR), including probiotics, prebiotics, synbiotics, postbiotics, and emerging approaches such as fecal microbiota transplantation, engineered microbes, and bacteriophage-based therapies. It examines proposed immunological mechanisms involving type 2 inflammation, regulatory immune pathways, and gut–airway axis signalling, while distinguishing clinically evaluated strategies from experimental or preclinical and assessing their translational readiness. Collectively, available evidence suggests that microbiome-targeted therapies represent a promising conceptual avenue for understanding and potentially modulating AR. However, their clinical application remains constrained by heterogeneous study designs, reliance on extrapolated data from preclinical studies, limited standardized outcome measures, insufficient long-term safety data, and evolving regulatory frameworks. Addressing these challenges through well-designed clinical trials and improved mechanistic characterization will be essential to clarify the role of microbiome-based interventions as adjunctive strategies in AR management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1765772</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1765772</link>
        <title><![CDATA[Treatment of toxic epidermal necrolysis in a patient with extensive skin damage induced by dimethyl N-cyanodithioiminocarbonate: a case report]]></title>
        <pubdate>2026-04-01T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Xiaokun Tian</author><author>Kai Zhang</author><author>Yingwei Qu</author><author>Bin Xu</author><author>Kaixin Cao</author><author>Cheng Wang</author>
        <description><![CDATA[IntroductionDimethyl N-cyanodithioiminocarbonate is a sulfur-containing industrial compound known to induce severe cutaneous reactions, including toxic epidermal necrolysis (TEN). Current management primarily focuses on immunomodulation, yet there is a recognized gap in standardized wound and systemic care for extensive, sepsis-complicated cases. This report describes a rarely documented case of dimethyl N-cyanodithioiminocarbonate-induced TEN involving over 90% of the total body surface area (TBSA) complicated by wound sepsis, and represents the application of a major-burn treatment protocol for this specific chemical-induced condition.Case presentationA 43-year-old male chemical plant worker presented with rapidly progressing skin detachment covering 92% TBSA and mucosal involvement, following occupational exposure without adequate protection. After initial dermatological management failed to prevent clinical deterioration, he was transferred to a burn intensive care unit (BICU). A multidisciplinary burn-oriented strategy was implemented, including: precise fluid resuscitation, gradual tapering of systemic corticosteroids, use of an air-fluidized bed, topical nano-silver dressings with compound purple grass oil, targeted antibiotics, and intensive nutritional support. Within two weeks, complete re-epithelialization was achieved without surgical intervention, and all infection markers normalized.ConclusionsThe integration of burn-critical care principles—particularly structured fluid resuscitation, pressure-offloading, and moist wound management—into the treatment of severe chemical-induced TEN can facilitate rapid wound closure and systemic recovery even in high-mortality-risk cases. This case supports the adoption of a multidisciplinary, burn-informed approach for extensive TEN and underscores the need for heightened occupational safety measures when handling potent sensitizers such as dimethyl N-cyanodithioiminocarbonate.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1788615</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1788615</link>
        <title><![CDATA[Concordance between different methods of detecting fungal-specific IgE antibody in asthma]]></title>
        <pubdate>2026-04-01T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Nadya Shifani</author><author>David W. Denning</author>
        <description><![CDATA[Documenting fungal sensitization plays a pivotal diagnostic role in asthma endotypes. Diagnosis relies heavily on detecting fungal-specific immunoglobulin E (sIgE), yet variability in allergen representation, cross-reactivity, and assay performance complicates standardization. Although ImmunoCAP is regarded as the reference method, many commercial kits are available worldwide, with varying accuracy. A scoping review was conducted using Arksey and O'Malley's five-stage framework. Literature searches in PubMed, Scopus, and ProQuest MEDLINE identified studies comparing fungal sIgE detection kits. Inclusion criteria required human studies evaluating fungal allergens in asthma-related diseases. Data from 16 eligible studies and 32 diagnostic kits were analyzed, focusing on assay characteristics, concordance, sensitivity, and specificity. There are 32 commercial kits available, which vary in detection principles, including enzyme immunoassays, immunoblots, and microarrays, with positivity thresholds ranging from 0.1 to 0.35 kUA/L. Most assays identified Aspergillus and Alternaria-specific IgE, while fewer detected Cladosporium, Candida, or Trichophyton. Concordance with ImmunoCAP ranged from moderate to substantial, with the strongest agreement reported for Alternaria. ImmunoCAP demonstrated the highest sensitivity and specificity; however, emerging systems, such as the GOLD chip and MeDALL microarray, showed promising improvements in multiplex capacity and detection limits. Meanwhile, several commercial assays have no publications documenting their diagnostic performance. Fungal sIgE detection remains heterogeneous. Newer microarray-based assays offer enhanced sensitivity and broader allergen profiling. Standardizing cutoff thresholds and incorporating recombinant fungal allergens are crucial for strengthening diagnostic precision and improving the clinical management of fungal asthma.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1798037</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1798037</link>
        <title><![CDATA[Chemokine ligand-receptor interactions as potential therapeutic targets for atopic dermatitis: from basic to clinical research]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Rio Tsukamoto</author><author>Hsi-Hua Chi</author><author>Hiroki Ueno</author><author>Shiena Tanaka</author><author>Shoko Fujiyoshi</author><author>Sung-Il Lee</author><author>Masanori A. Murayama</author>
        <description><![CDATA[Atopic dermatitis (AD) is a chronic inflammatory skin disease that commonly causes eczema accompanied by severe itching on pathological skin lesions. Although the pathological mechanisms are not fully understood, epidermal barrier dysfunction and immune dysfunction are critical for the development of AD. Notably, skin-infiltrating immune cells play a crucial role in the development of atopic skin inflammation. Recent studies have demonstrated that the infiltration of inflammatory cells into skin lesion is regulated by various chemokine ligands-receptors interactions. In this review, we focused on the pathogenic role of chemokines and chemokine receptors in AD development. The lesional skin tissues of patients with AD highly express various chemokines to enhance the migration of immune cells via chemokine ligand-receptor interactions. Since thier the inhibition and blockade contribute to the regulation of inflammatory response in the lesional skins of AD, chemokine ligands and/or receptors are prospective targets for AD therapy. In fact, some blocking agents and antagonist have shown positive results in the improvement of the inflammatory phenotypes in AD model mice. Clinical trials are progressing slowly but steadily, suggesting that chemokine ligands-receptors interactions remain a prospective therapeutic target for AD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/falgy.2026.1804294</guid>
        <link>https://www.frontiersin.org/articles/10.3389/falgy.2026.1804294</link>
        <title><![CDATA[Editorial: Anaphylaxis challenges: idiopathic and rare causes]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Maryam Ali Al-Nesf</author><author>Hassan Mobayed</author><author>Michael Makris</author><author>Iman Nasr</author><author>Ivan Cherrez-Ojeda</author><author>Luisa Ricciardi</author>
        <description></description>
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