Journal of Allergy and Clinical Immunology最新文献

{"title":"Epidemiology and management of malignancies in patients with inborn errors of immunity—An ESID registry study of 19,959 patients","authors":"Delfien J.A. Bogaert MD, PhD ,&nbsp;Christina H. Wolfsberger MD ,&nbsp;Andishe Attarbaschi MD ,&nbsp;Jonathan Gathmann ,&nbsp;Klaus Warnatz MD ,&nbsp;Gabriele Mueller ,&nbsp;Anna Mukhina MD ,&nbsp;Stephan Rusch DiplInf","doi":"10.1016/j.jaci.2025.10.033","DOIUrl":"10.1016/j.jaci.2025.10.033","url":null,"abstract":"<div><h3>Background</h3><div>Inborn errors of immunity (IEI), or primary immune disorders (PIDs), predispose individuals to infections, autoimmunity, inflammation, allergy, and malignancy. Malignancies are a major cause of morbidity and mortality in patients with IEI/PIDs, with poorer outcomes compared with the general population.</div></div><div><h3>Objective</h3><div>We sought to determine the frequency and types of malignancies in patients with IEI/PIDs and to assess clinical management approaches across Europe.</div></div><div><h3>Methods</h3><div>Descriptive analyses were performed on malignancy data within each IEI category. In addition, a European Society for Immunodeficiencies Registry survey (05/2022-03/2024) collected data on management strategies and challenges.</div></div><div><h3>Results</h3><div>Of 19,959 patients with IEI/PIDs, 1783 (8.9%) developed malignancies, of whom 27.1% presented malignancy as first manifestation of IEI/PIDs. A total of 1210 malignancies were specified; B-cell non-Hodgkin lymphoma was most common (24.2%). Detailed malignancy-IEI/PID association maps are provided. Predominantly antibody deficiencies accounted for 59.1% of malignancy cases, with a higher median age at first malignancy (43.6 years) compared with other IEI/PID categories, for example, combined immunodeficiencies with syndromic or associated features (11.7 years). Survey findings revealed that oncological treatment was modified because of IEI/PIDs in 21.5% of cases, with assumed negative impacts of IEI/PIDs on complications and outcomes (in 27.4% and 30.7%, respectively). IEI/PIDs influenced transplant decisions in 16.5% of cases. Management practices such as interdisciplinary decision finding and guideline availability were recorded.</div></div><div><h3>Conclusions</h3><div>This study provides comprehensive epidemiological data on malignancies in IEI/PIDs, highlighting the need for tailored screening and management. Survey results emphasize the real-world challenges and support the development of IEI/PID-specific oncological surveillance guidelines and treatment strategies.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 739-753"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534636","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":"High airway thymic stromal lymphopoietin in asthma is associated with type 2 inflammation, mucus plugging, and airway remodeling","authors":"Kritika Khanna PhD ,&nbsp;Monica Tang MD ,&nbsp;Nathan D. Jackson PhD ,&nbsp;Mats W. Johansson PhD ,&nbsp;Eugene R. Bleecker MD ,&nbsp;Mario Castro MD, MPH ,&nbsp;Suzy A. Comhair PhD ,&nbsp;Loren C. Denlinger MD, PhD ,&nbsp;Serpil C. Erzurum MD ,&nbsp;Annette T. Hastie PhD ,&nbsp;Wendy Moore MD ,&nbsp;Elliot Israel MD ,&nbsp;Bruce D. Levy MD ,&nbsp;Nizar N. Jarjour MD ,&nbsp;David T. Mauger PhD ,&nbsp;Brenda R. Phillips MS ,&nbsp;Kaharu Sumino MD, MPH ,&nbsp;Sally E. Wenzel MD ,&nbsp;Prescott G. Woodruff MD, MPH ,&nbsp;Max A. Seibold PhD ,&nbsp;John V. Fahy MD, MSc","doi":"10.1016/j.jaci.2025.11.014","DOIUrl":"10.1016/j.jaci.2025.11.014","url":null,"abstract":"<div><h3>Background</h3><div>Inhibition of thymic stromal lymphopoietin (TSLP) improves asthma control, but the relationships between airway TSLP levels and clinical and immunologic features of asthma are unclear.</div></div><div><h3>Objective</h3><div>We sought to determine associations between airway TSLP, disease control, and airway remodeling in asthma.</div></div><div><h3>Methods</h3><div>We measured TSLP protein in sputum from patients with mild-to-moderate asthma (University of California San Francisco cohort, n = 137), patients with moderate-to-severe asthma (Severe Asthma Research Program-3 cohort, n = 397), and healthy controls (n = 95). We explored how sputum TSLP levels relate to measures of lung function and exacerbations, airway inflammation, and lung image–based measures of mucus plugging and airway remodeling.</div></div><div><h3>Results</h3><div>The upper 95th percentile value for sputum TSLP concentration in healthy controls was 1.6 pg/mL; 16% of the University of California San Francisco cohort and 33.5% of the Severe Asthma Research Program-3 cohort had TSLP concentrations above this value. High sputum TSLP levels occurred most often in patients with severe asthma showing clinical traits typical of type 2 inflammation. There was considerable overlap between subgroups with high levels of TSLP and eosinophilic inflammation. High sputum TSLP levels were associated with a strong sputum cell gene expression profile for type 2 immune responses and a weak expression for type 1 responses. High sputum TSLP levels were also associated with high sputum <em>MUC5AC</em> expression and high scores for mucus plugging, air trapping, and other measures of airway remodeling on computed tomography lung scans.</div></div><div><h3>Conclusion</h3><div>High levels of airway TSLP in asthma are associated with more severe asthma with predominantly type 2 airway immune responses and with mucus plugging, air trapping, and airway remodeling.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 616-626"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145760091","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":"Sympathetic nerve dysfunction exacerbates skin inflammation in atopic dermatitis","authors":"Su Yu MD, PhD ,&nbsp;Yao Xu MD, PhD ,&nbsp;Yizhen Li MD ,&nbsp;Xiaoyu Pan MD ,&nbsp;Zixin Zhao BS ,&nbsp;Chaoying Gu MD, PhD ,&nbsp;Huibin Yin MD, PhD ,&nbsp;Qianwen Shan BS ,&nbsp;Yuemeng Wu MD, PhD ,&nbsp;Yu Wang MD, PhD ,&nbsp;Hao Wu MD, PhD ,&nbsp;Yehua Cai MD, MS ,&nbsp;Xu Yao MD, PhD ,&nbsp;Yan-Gang Sun PhD ,&nbsp;Wei Li MD, PhD","doi":"10.1016/j.jaci.2025.12.994","DOIUrl":"10.1016/j.jaci.2025.12.994","url":null,"abstract":"<div><h3>Background</h3><div>Atopic dermatitis (AD) is a chronic inflammatory skin disorder with severe itching, posing a great burden on both the physical and mental health of patients. AD is frequently complicated by sympathetic nervous system (SNS) dysfunction.</div></div><div><h3>Objective</h3><div>We sought to explore the interplay between skin inflammation and SNS activity during AD development.</div></div><div><h3>Methods</h3><div>Using clinical cohort data and murine models, we used impression mold technique, simultaneous noninvasive recording of electrocardiogram and skin sympathetic nerve activity, ultrasound, immunohistochemistry, and RNA sequencing to investigate the impact of AD inflammation on sympathetic function and structure. Conversely, chemogenetic manipulations were used to assess the effects of the SNS on AD-related inflammation and itch.</div></div><div><h3>Results</h3><div>We revealed significant SNS dysfunction in patients with AD, which was manifested by diminished perspiration and attenuated electrical responses, and ultrasound data showed compensatory hypertrophy in the sympathetic ganglia. These impairments were partially reversed in patients with AD treated with dupilumab. Moreover, MC903-induced AD-like dermatitis exhibited histologic and molecular indications of inflammatory stress and injury in the sympathetic ganglia. Chemogenetic inhibition of <em>Phox2b</em>^<em>+</em> sympathetic neurons exacerbated MC903-induced cutaneous inflammation and itch sensation in mice, whereas targeted activation of sympathetic neurons attenuated both clinical and histologic manifestations of AD-like dermatitis.</div></div><div><h3>Conclusions</h3><div>Our data revealed a detrimental cycle between AD skin inflammation and sympathetic nerve dysfunction.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 677-692"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145822998","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":"Targeting IL-22RA1 with temtokibart: A novel approach in atopic dermatitis: Phase 2a monotherapy study results","authors":"Diamant Thaçi MD ,&nbsp;Vivian Laquer MD ,&nbsp;Charles Lynde MD ,&nbsp;Adam Reich MD, PhD ,&nbsp;Weily Soong MD ,&nbsp;Margitta Worm MD ,&nbsp;Petra Arlert PhD ,&nbsp;Allan Blemings MSc ,&nbsp;Thomas Litman PhD ,&nbsp;Britta C. Martel PhD ,&nbsp;Martin Olesen MD, PhD ,&nbsp;Ole E. Sørensen MD, PhD ,&nbsp;Melinda Gooderham MD","doi":"10.1016/j.jaci.2025.08.034","DOIUrl":"10.1016/j.jaci.2025.08.034","url":null,"abstract":"<div><h3>Background</h3><div>Atopic dermatitis (AD) is a chronic inflammatory skin disease in which increased IL-22 expression contributes to epidermal hyperplasia and barrier defects. Temtokibart is a monoclonal antibody targeting IL-22RA1 (IL-22 receptor subunit alpha-1), blocking the signaling of IL-22 and potentially also of IL-20 and IL-24.</div></div><div><h3>Objective</h3><div>We evaluated the efficacy and safety of temtokibart in adults with moderate-to-severe AD.</div></div><div><h3>Methods</h3><div>In this phase 2a study (NCT04922021), 58 adults were randomized 1:1 to subcutaneous temtokibart 450 mg or placebo every 2 weeks for 16 weeks, with an additional dose (450 mg) at week 1, followed by additional 16 weeks of safety follow-up. The primary end point was change in Eczema Area Severity Index (EASI) from baseline to week 16. Biomarkers in serum, including IL-22, were analyzed as an exploratory end point.</div></div><div><h3>Results</h3><div>Mean change in EASI from baseline to week 16 was significantly greater for temtokibart compared to placebo (−15.3 vs −3.5; <em>P</em> = .003), corresponding to 65.4% and 19.7% improvement for temtokibart and placebo groups, respectively. At week 16, greater proportions of patients receiving temtokibart relative to placebo obtained EASI-75 (41.6% vs 13.7%; <em>P</em> = .011), EASI-90 (30.8% vs 3.5%; <em>P</em> = .003), and EASI-100 (20.9% vs 0%; <em>P</em> = .006). Treatment with temtokibart was well tolerated, and no safety signals were observed. Further, temtokibart treatment was associated with a general reduction of systemic inflammatory proteins.</div></div><div><h3>Conclusions</h3><div>This proof-of-concept study demonstrates that targeting the IL-22 pathway with temtokibart is clinically effective with a favorable safety profile.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 666-676"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498676","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":"Sex hormones influence ORMDL3 expression: Implications for sex-associated asthma phenotype","authors":"Elisabetta Granato PhD ,&nbsp;Ida Cerqua PhD ,&nbsp;Antonietta Rossi PhD ,&nbsp;Maria Antonietta Riemma PhD ,&nbsp;Maria Chiara Monti PhD ,&nbsp;Giusy Ferraro PhD ,&nbsp;Barbara Romano PhD ,&nbsp;Maria Francesca Nanì PhD ,&nbsp;Danilo D’Avino PhD ,&nbsp;Martina Simonelli PhD ,&nbsp;Joshua Malo MD ,&nbsp;Francesca Polverino MD, PhD ,&nbsp;Bruno D’Agostino MD ,&nbsp;Giuseppe Cirino PhD ,&nbsp;Fiorentina Roviezzo PhD","doi":"10.1016/j.jaci.2025.10.035","DOIUrl":"10.1016/j.jaci.2025.10.035","url":null,"abstract":"<div><h3>Background</h3><div>Genetic polymorphisms in sphingolipid metabolism, particularly involving the orosomucoid-like 3 <em>(ORMDL3)</em> gene, have been associated with asthma risk. Notably, asthma prevalence and severity exhibit pronounced sex differences, emerging in childhood and persisting into adulthood. However, the molecular mechanisms underlying this sexual dimorphism remain incompletely elucidated.</div></div><div><h3>Objective</h3><div>We investigated whether <em>ORMDL3</em> contributes to sex differences in airway function and asthma-like features.</div></div><div><h3>Methods</h3><div><em>ORMDL3</em> expression was measured in lung tissues from healthy male and female human donors and in human bronchial epithelial cells (BEAS-2B) after exposure to 17β-estradiol (E2), <em>Dermatophagoides pteronyssinus</em> 1 (Der p 1), or both. A murine preparation of asthma was used to evaluate sex-dependent differences in <em>ORMDL3</em> expression, airway responsiveness, and remodeling. Pharmacologic modulation of estrogen signaling and the ORMDL3–sphingosine-1-phosphate (S1P) axis were used. Methods included quantitative real-time PCR, immunostaining, liquid chromatography–tandem mass spectrometry, and airway function measurements.</div></div><div><h3>Results</h3><div>Female lungs exhibited higher <em>ORMDL3</em> expression than male lungs, and this correlated with elevated forced expiratory volume to forced vital capacity ratios in the same patients. In BEAS-2B cells, E2 significantly upregulated ORMDL3 and altered sphingolipid metabolism by inducing expression of ceramidase, sphingosine kinases 1/2, and S1P receptors. Der p 1 also increased ORMDL3 and triggered epithelial activation via inflammasome signaling, while E2 enhanced IFN-β signaling and <em>MUC5AC</em> expression. Combination Der p 1/E2 synergistically activated sphingolipid, interferon, and inflammasome pathways. These <em>in vitro</em> findings prompted <em>in vivo</em> investigation using a murine asthma preparation, where female mice displayed elevated ORMDL3, sphingosine, and S1P levels, with increased airway hyperresponsiveness and remodeling. Treatment with tamoxifen or E2 normalized airway hyperresponsiveness and S1P signaling across sexes. Allergen sensitization intensified female-biased <em>ORMDL3</em> expression and airway inflammation. Inhibition of the ORMDL3-S1P axis attenuated asthma-like features only in female animals.</div></div><div><h3>Conclusion</h3><div>This study identifies ORMDL3 as an estrogen-responsive regulator of airway responsiveness that may contribute to sex-related differences in asthma features through modulation of sphingolipid metabolism.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 602-615.e7"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689940","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":"Running out of air: Loss of hypoxia-inducible factor and CD73-dependent repair in eosinophilic esophagitis","authors":"Edsel M. Abud MD, PhD ,&nbsp;Seema S. Aceves MD, PhD","doi":"10.1016/j.jaci.2026.01.005","DOIUrl":"10.1016/j.jaci.2026.01.005","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 599-601"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033212","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":"CME Calendar-AAAAI","authors":"","doi":"10.1016/S0091-6749(26)00047-3","DOIUrl":"10.1016/S0091-6749(26)00047-3","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages A29-A30"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147334785","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":"Aberrant ceramide accumulation fuels eosinophilic inflammation by promoting eosinophil extracellular trap formation and release in chronic rhinosinusitis with nasal polyps","authors":"Pengda Fang MD ,&nbsp;Mengzhen Wu MD ,&nbsp;Junhai Chen MD ,&nbsp;Wenlong Li MD ,&nbsp;Yurong Bai MD, PhD ,&nbsp;Wenyi Chen BS ,&nbsp;Yue Li MD, PhD ,&nbsp;Xinyue Wang MD, PhD ,&nbsp;Zhenhao Xiao MD ,&nbsp;Tong Wu BS ,&nbsp;Qintai Yang MD, PhD ,&nbsp;Yana Zhang MD, PhD","doi":"10.1016/j.jaci.2025.11.004","DOIUrl":"10.1016/j.jaci.2025.11.004","url":null,"abstract":"<div><h3>Background</h3><div>Eosinophilic inflammation represents a hallmark pathologic feature of chronic rhinosinusitis with nasal polyps (CRSwNP). Although ceramides, the central sphingolipid metabolites, are implicated in asthma pathogenesis, their mechanistic contributions to CRSwNP remain poorly elucidated.</div></div><div><h3>Objective</h3><div>We sought to investigate the functions and associated mechanisms of ceramide in the pathogenesis of CRSwNP.</div></div><div><h3>Methods</h3><div>Immunofluorescence and absolute quantitative lipidomics analysis were performed to evaluate the levels of ceramide and its species in nasal biopsy samples. <em>In vitro</em> culture and stimulation of purified eosinophils from human peripheral blood to validate the function of ceramides. Small interfering RNA transfection and inhibition assays to determine the molecular mechanism.</div></div><div><h3>Results</h3><div>The expression levels of ceramide and its binding protein were enriched in eosinophilic CRSwNP. Increased Cer(18:1_24:1) was related with eosinophil extracellular trap (EET) counts and disease severity in patients with eosinophilic CRSwNP. Cer(18:1_24:1) potently induced eosinophils activation by promoting EET formation and release. Mechanistically, Cer(18:1_24:1)-induced elevated levels of reactive oxygen species (ROS)/mitochondrial ROS (mROS) promoted EET formation by upregulating PAD4/CitH3 on one hand, and drove the oligomerization of the N terminal of gasdermin D (GSDMD-N) and membrane pore formation to facilitate the EET release on the other hand. Furthermore, ceramide-binding protein PP2AC inhibition blocked EET formation and release by reduction of ROS/mROS production. Interestingly, selenium supplementation mitigated Cer(18:1_24:1)-induced EET production and release by decreasing production of ROS/mROS.</div></div><div><h3>Conclusions</h3><div>Aberrant ceramide accumulation fuels eosinophilic inflammation by promoting EET formation and release through the PP2AC-ROS/mROS-GSDMD-N pathway, which may contribute to the severity and progression of eosinophilic CRSwNP. These mechanistic insights may provide novel therapeutic strategies for eosinophil-driven inflammatory disorders.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 636-652"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145567234","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":"Mechanistic insights into petechiae observed with remibrutinib therapy in chronic spontaneous urticaria","authors":"Raquel Lazarowitz MD(c) ,&nbsp;Giselle Mosnaim MD, MSc ,&nbsp;Michael Fein MD, MSc ,&nbsp;Anna Nikonova MD ,&nbsp;Elena Netchiporouk MD, MSc","doi":"10.1016/j.jaci.2025.12.997","DOIUrl":"10.1016/j.jaci.2025.12.997","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 782-783"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933395","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":"Information for Readers","authors":"","doi":"10.1016/S0091-6749(26)00045-X","DOIUrl":"10.1016/S0091-6749(26)00045-X","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Page A25"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147334355","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}