Journal of Allergy and Clinical Immunology最新文献

{"title":"The 2024 Nobel Prizes: AI and computational science take center stage.","authors":"Nicholas L Rider, Mohamed Shamji","doi":"10.1016/j.jaci.2024.11.040","DOIUrl":"10.1016/j.jaci.2024.11.040","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monocytic reactive oxygen species-induced T cell apoptosis impairs cellular immune response to SARS-CoV-2 mRNA vaccine.","authors":"Sandrine Gimenez, Emna Hamrouni, Sonia André, Morgane Picard, Calayselvy Soundaramourty, Claire Lozano, Thierry Vincent, Tu-Anh Tran, Lucy Kundura, Jérôme Estaquier, Pierre Corbeau","doi":"10.1016/j.jaci.2025.01.003","DOIUrl":"https://doi.org/10.1016/j.jaci.2025.01.003","url":null,"abstract":"<p><strong>Background: </strong>We have recently shown that, during acute severe COVID-19, SARS-CoV-2 spike protein (S) induces a cascade of events resulting in T cell apoptosis. Indeed, by neutralizing the protease activity of its receptor, ACE2, S induces an increase in circulating Angiotensin II (AngII), resulting in monocytic release of reactive oxygen species (ROS) and programmed T cell death.</p><p><strong>Objective: </strong>Here, we tested whether SARS-CoV-2 mRNA vaccines, known to cause the circulation of the vaccine antigen, S-protein receptor binding domain (RBD), might trigger the same cascade.</p><p><strong>Methods: </strong>To this aim, we used ELISA to quantify the presence of RBD and AngII in participants' peripheral blood as well as the presence of interferon-γ in the supernatant of peripheral blood mononuclear cells (PBMCs) exposed to S. Monocytic ROS production, T cell apoptosis, and S-induced T lymphocyte proliferation were measured by flow cytometry, and DNA damage by immunofluorescence.</p><p><strong>Results: </strong>In most vaccinees, we observed the presence of circulating RBD peaking on Day 14, and linked to an increase in AngII plasma levels with a peak on Day 28. This increase correlated with i) the ability of monocytes to produce ROS and to induce ROS-mediated DNA damage in neighboring cells, including PBMCs, ii) CD4⁺ and CD8⁺ T lymphocyte apoptosis, and iii) a poor response to S in vitro from both CD4⁺ and CD8⁺ T cells.</p><p><strong>Clinical implications: </strong>We observed the same cascade of events triggered by the vaccinal antigen as by SARS-CoV-2 infection. This cascade may account for the suboptimal efficiency of mRNA SARS-CoV-2 vaccines in preventing the infection, the limited vaccine memory, and certain side-effects. In this model, AngII receptor antagonists and/or antioxidants might improve the performance of the SARS-CoV-2 vaccine.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Bronchial Epithelial Genes Associated with Type-2 Eosinophilic Inflammation in Asthma.","authors":"Stephane Esnault, Kimberly A Dill-McFarland, Matthew C Altman, Melissa A Rosenkranz, Nizar N Jarjour, William W Busse","doi":"10.1016/j.jaci.2024.12.1089","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.12.1089","url":null,"abstract":"<p><strong>Background: </strong>Airway inflammation has a critical role in asthma pathogenesis and pathophysiology. Yet, the molecular pathways contributing to airway inflammation are not fully known, particularly Type-2 (T2) inflammation characterized by both eosinophilia and higher FeNO levels.</p><p><strong>Objective: </strong>To identify genes whose level of expression in epithelial brushing samples were associated with both bronchoalveolar lavage (BAL) eosinophilia and generation of FeNO.</p><p><strong>Methods: </strong>We performed segmental allergen bronchoprovocation (SBP-Ag) in participants with asthma, and RNA-sequencing (RNA-seq) analyses of BAL cells and brushing samples before and 48 h after SBP-Ag to identify regulation of eosinophil recruitment and FeNO changes.</p><p><strong>Results: </strong>Allergen bronchoprovocation increased FeNO levels, which correlated with eosinophilia. Thirteen genes were identified in brushing samples, whose expression changed in response to SBP-Ag and correlated with both airway eosinophilia and FeNO levels after SBP-Ag. Among these 13 genes, the epithelial cell product, CDH26/cadherin-26 contributed to the amplification of T2 inflammation, as reflected by eosinophilia and FeNO, and causal mediation analyses with pro-T2 and pro-eosinophilic cytokine mediators in BAL fluids. Among the genes associated with reduced eosinophilia and FeNO, HEY2 is known to enhance cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT), as well as to reduce apoptosis.</p><p><strong>Conclusion: </strong>This unbiased RNA-seq analysis in participants with allergic asthma revealed several epithelial cell genes, particularly CDH26, that may be critical for the development or augmentation of T2 inflammation in asthma.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic profiling of chronic hand eczema skin reveals shared immune pathways and molecular drivers across subtypes.","authors":"Anna Sophie Quaade, Thomas Litman, Xing Wang, Christine Becker, Benjamin D McCauley, Julie Breinholt Kjær Sølberg, Jacob P Thyssen, Jeanne Duus Johansen","doi":"10.1016/j.jaci.2024.12.1091","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.12.1091","url":null,"abstract":"<p><strong>Background: </strong>Chronic hand eczema (CHE) is a common skin disease with different subtypes, but knowledge of the molecular patterns associated with each subtype is limited.</p><p><strong>Objective: </strong>To characterize the CHE transcriptome across subtypes.</p><p><strong>Methods: </strong>Using RNA-sequencing, we studied the transcriptome of 220 full-thickness skin biopsies collected from palms, dorsa, and arms from 96 patients with CHE and/or atopic dermatitis (AD) and 32 healthy controls. The primary analysis focused on 16 healthy and 54 lesional CHE palm samples that were further stratified by AD status and unique etiology. Differentially expressed genes (DEGs) were identified across the cohort and Ingenuity pathway analysis (IPA) was used for pathway analysis and upstream regulator prediction.</p><p><strong>Results: </strong>We identified anatomical site-specific transcriptomic variations, showing unique characteristics in both healthy and CHE-affected palm skin. In CHE palms, we identified 2333 DEGs versus healthy palms. Upregulated genes predominantly involved keratinocyte host inflammation and immune signaling, while downregulated genes were linked to lipid metabolism and epidermal barrier function. IPA revealed numerous activated pro-inflammatory pathways, dominated by Th1 and Th2. Key upstream regulators included type 1 (IFNG, TNF, STAT1, IL-2) and type 2 (IL-4) associated molecules, and IL-1β. Lesional palm signatures were broadly shared across CHE subtypes. No DEGs were found between allergic- and irritant contact dermatitis CHE. Subtype-specific pathway and upstream regulator activity variations were noted.</p><p><strong>Conclusion: </strong>The lesional CHE transcriptome is primarily shared among subtypes and is characterized by activation of several immune pathways, dominated by Th1 and Th2. Key shared upstream regulators were identified, highlighting potential universal therapeutic targets.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of Airway and Systemic Interferon Responses Promote Asthma Exacerbations in Urban Children.","authors":"Courtney L Gaberino, Matthew C Altman, Michelle A Gill, Leonard B Bacharier, Rebecca S Gruchalla, George T O'Connor, Rajesh Kumar, Gurjit K Khurana Hershey, Meyer Kattan, Andrew H Liu, Stephen J Teach, Edward M Zoratti, Patrice M Becker, Alkis Togias, Cynthia Visness, James E Gern, William W Busse, Daniel J Jackson","doi":"10.1016/j.jaci.2024.12.1090","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.12.1090","url":null,"abstract":"<p><strong>Background: </strong>Determining why some upper respiratory illnesses provoke asthma exacerbations remains an unmet need.</p><p><strong>Objective: </strong>To identify transcriptome-wide gene expression changes associated with colds that progress to exacerbation.</p><p><strong>Methods: </strong>208 urban children (6-17 years) with exacerbation-prone asthma were prospectively monitored for up to two cold illnesses. Exacerbation illnesses (Ex+), defined as colds leading to asthma exacerbations requiring systemic corticosteroids within 10 days, were compared to colds that resolved without exacerbation (Ex-). Peripheral blood and nasal lavage samples were collected at baseline and during colds for RNA sequencing. Interferon gene expression was compared between Ex+ and Ex- illnesses. Generalized additive modeling revealed interferon response kinetics. Multiple linear regression models compared interferon expression to clinical variables.</p><p><strong>Results: </strong>106 participants were evaluated during 154 colds. There was greater up-regulation of differentially expressed interferon genes during Ex+ illnesses compared to Ex-. Ex+ illnesses had greater average and steeper rise in interferon expression. Within three days of illness, interferon expression was positively associated with nasal rhinovirus quantity (nasal:adjustedR²=0.48, p=0.015; blood:adjustedR²=0.22, p=0.013) and interferon expression was negatively associated with FEV₁ percent predicted (nasal:β=-0.010, p=0.048; blood:β=-0.008, p=0.023). Participants with lower baseline interferon expression had shorter time to exacerbation, higher risk for exacerbation with viral illnesses and greater increase in interferon expression during viral colds (nasal:β=-0.80, p<0.0001; blood:β=-0.75, p<0.0001).</p><p><strong>Conclusion: </strong>Dysregulated interferon responses are important contributors to asthma exacerbation risk in children. Low baseline interferon expression followed by greater up-regulation of interferon pathways in airway and blood during respiratory illnesses increased exacerbation risk. Targeting this pathway in at-risk individuals holds promise for the personalized prevention of asthma exacerbations.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mepolizumab in patients with lymphoid variant hypereosinophilic syndrome: a multi-center prospective study.","authors":"Julien Catherine, Sina Karimi, Laurent Dewispelaere, Christophe Lelubre, Liliane Schandené, Florence Roufosse","doi":"10.1016/j.jaci.2024.12.1085","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.12.1085","url":null,"abstract":"<p><strong>Background: </strong>Hypereosinophilic syndrome (HES) is characterized by blood and tissue hypereosinophilia causing organ damage and/or dysfunction. Mepolizumab, an anti-IL-5 antibody, has recently been approved in this indication. In lymphoid variant (L-)HES, eosinophil expansion is driven by IL-5-producing clonal CD3^-CD4⁺ T cells.</p><p><strong>Objective: </strong>This study aimed to elucidate the efficacy of mepolizumab in patients with CD3^-CD4⁺ L-HES, and the impact of treatment on aberrant cells and associated biomarkers.</p><p><strong>Methods: </strong>A biomarker sub-study was conducted during two clinical trials evaluating mepolizumab in HES, a 32-week randomized placebo-controlled trial (200622) followed by a 20-week open-label extension (205203). Patients with CD3^-CD4⁺ and/or clonal T cells, elevated serum TARC/CCL17, sCD25 and/or detectable IL-5 were identified, and their treatment responses were compared to those without these anomalies.</p><p><strong>Results: </strong>Of the 108 patients enrolled in 200622-205203, 103 consented to this study, including 17 with a CD3^-CD4⁺ T-cell subset. Presence of CD3^-CD4⁺ T cells or sCD25 levels ≥1500 pg/ml was associated with reduced eosinophil-lowering and corticosteroid-sparing effects of mepolizumab. None of the biomarkers were associated with an increased likelihood of experiencing clinical flares. A mepolizumab-induced increase in serum IL-5 was observed, that was significantly higher in patients with CD3^-CD4⁺ T cells. Treatment did not affect CD3^-CD4⁺ T cell counts.</p><p><strong>Conclusion: </strong>Mepolizumab has a favorable impact on disease flares in patients with CD3^-CD4⁺ L-HES, although reduced eosinophil-depleting and corticosteroid-sparing effects are observed at the currently-approved dose. Further studies are needed to validate these findings on larger patient cohorts, and to explore whether clinical activity other than flares is equally controlled in this disease variant.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Examining disparities in biologic therapy initiation: The intersection of race/ethnicity and insurance type.","authors":"Khamron Micheals,Darlene Bhavnani,Elizabeth C Matsui","doi":"10.1016/j.jaci.2025.01.002","DOIUrl":"https://doi.org/10.1016/j.jaci.2025.01.002","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"44 1","pages":""},"PeriodicalIF":14.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhinoconjunctivitis Symptoms in Children and Adolescents with Asthma: A Longitudinal Clustering Analysis.","authors":"Alkis Togias, Peter J Gergen, Andrew H Liu, Haejin Kim, Robert A Wood, George T O'Connor, Melanie Makhija, Gurjit K Khurana Hershey, Carolyn M Kercsmar, Rebecca S Gruchalla, Carin Lamm, Leonard B Bacharier, Shilpa J Patel, James E Gern, Daniel J Jackson, Cindy Visness, Agustin Calatroni, William W Busse","doi":"10.1016/j.jaci.2024.12.1084","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.12.1084","url":null,"abstract":"<p><strong>Background: </strong>Rhinoconjunctivitis phenotypes are conventionally described based on symptom severity, duration and seasonality and aeroallergen sensitization. It is not known whether these phenotypes fully reflect the patterns of symptoms seen at a population level.</p><p><strong>Objective: </strong>To identify phenotypes of rhinoconjunctivitis based on symptom intensity and seasonality using an unbiased approach and to compare their characteristics.</p><p><strong>Methods: </strong>A cohort of children with asthma in low-income urban environments was prospectively followed with a rhinoconjunctivitis activity questionnaire and their upper and lower airway disease was managed for 12 months with every 2-month visits based on standardized algorithms. We identified individual rhinoconjunctivitis symptom trajectories and clusters of those trajectories and compared the clusters focusing on atopic characteristics.</p><p><strong>Results: </strong>Data obtained from 619 children yielded 5 symptom clusters: two had high symptoms (22.5%) but differed in seasonal pattern, one had medium symptoms (13.6%), one had medium nasal congestion only (20.4%) and one had low symptoms (43.6%). The latter was further split into two subgroups if nasal corticosteroids were frequently prescribed (23.6%) or not (20.0%). Seasonal variation was absent in the low symptom clusters. The number of allergic sensitizations and family history of allergic airway disease were higher in the high symptom clusters, but allergic sensitization did not explain differences in seasonality.</p><p><strong>Conclusions: </strong>This study identified rhinoconjunctivitis phenotypes that have not been previously reported and were not differentiated by demographics, or measures of atopy and type 2 inflammation. Factors beyond allergy need to be investigated to better understand the pathobiology of rhinoconjunctivitis.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dupilumab reduces inflammatory biomarkers in pediatric patients with moderate-to-severe atopic dermatitis.","authors":"Lisa A Beck, Antonella Muraro, Mark Boguniewicz, Zhen Chen, Joseph Zahn, Ainara Rodríguez Marco","doi":"10.1016/j.jaci.2024.08.005","DOIUrl":"10.1016/j.jaci.2024.08.005","url":null,"abstract":"<p><strong>Background: </strong>Patients with atopic dermatitis (AD) often have elevated type 2 inflammatory serum biomarkers.</p><p><strong>Objective: </strong>The aim was to report changes in thymus and activation-regulated chemokine (TARC)/CC chemokine ligand 17 (CCL17), total IgE, lactate dehydrogenase (LDH), and eosinophils in pediatric patients treated with dupilumab or placebo.</p><p><strong>Methods: </strong>Biomarker data were analyzed from 3 randomized, double-blind, placebo-controlled, phase 3 studies of patients with moderate-to-severe AD. Patients ages 6 months to 5 years were randomly assigned to weight-dependent dupilumab 200/300 mg every 4 weeks (q4w) or placebo; ages 6 to 11 years, to dupilumab 100/200 mg every 2 weeks (q2w), dupilumab 300 mg q4w, or placebo; ages 12 to 17 years, to dupilumab 200/300 mg q2w, dupilumab 300 mg q4w, or placebo. In the youngest 2 groups, topical corticosteroids were also applied. Median percent changes from baseline to week 16 were reported using last observation carried forward analysis, censoring after rescue treatment.</p><p><strong>Results: </strong>Pediatric patients who received dupilumab versus placebo achieved significantly greater median percent reductions at week 16 in TARC/CCL17 (-83.3% to -72.4% vs -14.9% to -1.8%), total IgE (-71.2% to -58.4% vs -21.0% to +28.1%), and LDH (-26.2% to -9.8% vs -1.5% to +1.5%). All comparisons were significantly different (P < .0001) between each dupilumab dosing group and respective placebo groups. In contrast, absolute changes in eosinophils were small in all groups.</p><p><strong>Conclusions: </strong>Dupilumab treatment for pediatric patients with moderate-to-severe AD significantly reduced levels of TARC/CCL17, total IgE, and LDH to levels comparable with those of healthy controls, reflecting a reduction in systemic type 2 and general inflammation.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":"135-143"},"PeriodicalIF":11.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142046718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Updated review of omalizumab to treat uncontrolled pediatric allergic asthma.","authors":"Bradley E Chipps, Meghan Farrell Garcia, Kevin R Murphy, Tmirah Haselkorn","doi":"10.1016/j.jaci.2024.11.013","DOIUrl":"10.1016/j.jaci.2024.11.013","url":null,"abstract":"<p><p>Asthma has been increasingly recognized as a heterogeneous disease; however, many patients with asthma have allergic asthma (AA). Inhaled corticosteroids and other inhalers have been integral in treating many symptoms of asthma, but these medications do not completely address the disease's underlying mechanism. Pediatric asthma imposes a substantial burden on patients and the health care system. Omalizumab is consistently recognized as an important consideration for add-on therapy in pediatric patients with AA in published guidelines from multiple international societies such as the Global Initiative for Asthma. Since our last report in 2017, the amount of information available regarding the safety and effectiveness of omalizumab in pediatric patients with AA has continued to accumulate and is supported by several observational and real-world data studies. A number of studies including real-world effectiveness studies, post hoc analyses of clinical trial data, and systematic literature reviews and meta-analyses have since expanded the published data on the efficacy and safety of omalizumab in pediatric patients. In this article, we present an updated review of this literature focused on omalizumab therapy in children with AA.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":" ","pages":"12-23"},"PeriodicalIF":11.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}