Journal of Allergy and Clinical Immunology最新文献

{"title":"CME Calendar-AAAAI","authors":"","doi":"10.1016/S0091-6749(26)00604-4","DOIUrl":"10.1016/S0091-6749(26)00604-4","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages A25-A26"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149095604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrolides for asthma: A systematic review and meta-analysis of randomized trials","authors":"Leonardo M. Ologundudu BHSc,&nbsp;Melanie M. Wong MD,&nbsp;Nazmul Islam MPH,&nbsp;Daniel G. Rayner MSc,&nbsp;Alexandro W.L. Chu MD,&nbsp;Mark Loeb MD,&nbsp;Katherine Rivera-Spoljaric MD, MSCI,&nbsp;Bradley Chipps MD,&nbsp;Kaharu Sumino MD,&nbsp;John Oppenheimer MD,&nbsp;Sharmilee M. Nyenhuis MD,&nbsp;Elliot Israel MD,&nbsp;Flavia Hoyte MD,&nbsp;Tamara T. Perry MD,&nbsp;Ellen McCabe PhD,&nbsp;Valerie G. Press MD, MPH,&nbsp;Susana Rangel MSN, FNP-C,&nbsp;Gordon H. Guyatt MD,&nbsp;Lindsay E. Shade MHS PA-C,&nbsp;Paul M. O’Byrne MBChB,&nbsp;Derek K. Chu MD, PhD","doi":"10.1016/j.jaci.2026.01.024","DOIUrl":"10.1016/j.jaci.2026.01.024","url":null,"abstract":"<div><h3>Background</h3><div>The benefits and harms of using macrolides for asthma remain unclear.</div></div><div><h3>Objective</h3><div>As part of upcoming Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters guidelines addressing severe asthma, we systematically reviewed the efficacy and safety of macrolides for asthma.</div></div><div><h3>Methods</h3><div>We systematically searched MEDLINE, Embase, and CENTRAL to April 12, 2025, for randomized trials comparing macrolides with placebo or standard care for asthma. Paired reviewers independently screened records and extracted data. Individual patient-level data in random effects analysis of covariance models addressed asthma control and asthma-related quality of life. Random effects meta-analyses addressed severe exacerbations and harms. We used the Grading of Recommendations Assessment, Development and Evaluation approach to evaluate certainty of evidence. Our study protocol is registered in PROSPERO (CRD42023408677).</div></div><div><h3>Results</h3><div>Our meta-analysis comprised 19 trials enrolling 1825 participants. Compared with placebo, macrolides improve asthma control (6-item Asthma Control Questionnaire; score range 0-6, lower better; between-group mean difference: −0.23 [95% CI −0.32 to −0.13]; 40.6% vs 21.6% improving by minimally important difference of 0.5 point; high certainty), likely reduce severe exacerbations (incidence rate ratio: 0.75 [95% CI 0.57 to 0.98]; rate difference: 0.26 fewer events per patient-year [95% CI 0.45 to 0.02 fewer events]; moderate certainty), and likely modestly improve quality of life (Asthma Quality of Life Questionnaire; score range 1-7, higher better; mean difference: 0.11 [95% CI −0.06 to 0.29]; 47.6% vs 42.4% improving by minimally important difference of 0.5 points; moderate certainty) with little to no effect on serious adverse events and mortality (high certainty). Relative effects were similar among patients with type 2 high inflammation versus type 2 low inflammation asthma.</div></div><div><h3>Conclusions</h3><div>Macrolides likely reduce severe exacerbations and improve asthma control and quality of life with little to no difference in serious harms among patients with type 2 high inflammation or type 2 low inflammation asthma.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 970-981"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146134411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B-cell dysregulation and broad autoantibody repertoire underlie the immunopathology of MIS-C","authors":"Sakshi Malik PhD,&nbsp;Deepak Kumar PhD,&nbsp;Chengyu Prince BS,&nbsp;Thinh H. Nguyen MD, PhD,&nbsp;Christina A. Rostad MD,&nbsp;Taylor Fitch MD,&nbsp;Preeti Jaggi MD,&nbsp;D. Sofia Villacis Nunez MD,&nbsp;Lori A. Ponder BS,&nbsp;Michael Briones DO,&nbsp;Shaohui Hu PhD,&nbsp;Tyler Hulett PhD,&nbsp;Sampath Prahalad MD,&nbsp;Shanmuganathan Chandrakasan MD","doi":"10.1016/j.jaci.2026.07.004","DOIUrl":"10.1016/j.jaci.2026.07.004","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 1152-1156"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678336","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":"Maternal antibiotic exposure alters the newborn metabolomic profile and increases the risk of respiratory infections in offspring: A 13-year longitudinal birth cohort study","authors":"Marie Hauerslev MD, PhD,&nbsp;Tingting Wang MSc, PhD,&nbsp;Anton Kjellberg MSc,&nbsp;Yang Luo MSc, PhD,&nbsp;Jonathan Thorsen MD, PhD,&nbsp;Susanne Brix MSc, PhD,&nbsp;Tamo Sultan MD,&nbsp;Søren Sørensen MSc, PhD,&nbsp;Madeleine Ernst MSc, PhD,&nbsp;Jakob Stokholm MD, PhD,&nbsp;Klaus Bønnelykke MD, PhD,&nbsp;Bo Chawes MD, PhD, DMSc,&nbsp;Nicklas Brustad MD, PhD","doi":"10.1016/j.jaci.2026.05.034","DOIUrl":"10.1016/j.jaci.2026.05.034","url":null,"abstract":"<div><h3>Background</h3><div>Maternal antibiotic exposure during pregnancy has been associated with early childhood infection proneness, but the underlying mechanisms remain unknown. Longitudinal birth cohort studies with long follow-up and multiomics data are lacking.</div></div><div><h3>Objective</h3><div>We investigated the association between prenatal antibiotics and offspring infection risk as well as its potential mechanisms.</div></div><div><h3>Methods</h3><div>The Danish population-based COPSAC₂₀₁₀ cohort with 663 mother–child pairs was followed from pregnancy until child age 13 years. Detailed infection diaries were reviewed for age 0-3 years for common infections (cold, tonsillitis, otitis media, fever, gastrointestinal infections, and pneumonia), and moderate-to-severe (hospital diagnoses) infections were registered until age 13 years. We analyzed maternal antibiotic exposure versus risk of offspring infection risk with assessments of newborn child blood metabolome, gut and airway (age 1 week and 1 month) microbiome, and airway cytokine profiles (age 1 month). We adjusted for genetic, environmental, and socioeconomic factors.</div></div><div><h3>Results</h3><div>Children whose mothers were exposed to antibiotics during pregnancy had a higher risk of infections until age 13 years, with an adjusted incidence rate ratio of 1.75 (95% confidence interval, 1.19-2.57; <em>P</em> = .005), and pneumonia, with an adjusted incidence rate ratio of 1.81 (95% confidence interval, 1.10-2.99; <em>P</em> = .015). Maternal antibiotic exposure–related changes in the newborn child metabolome profile associated with increased child pneumonia, tonsilitis, and fever risk. Both number and types of maternal antibiotic treatments affected offspring infection risk. There were no noticeable findings for microbiome, genetics, and airway cytokine profiling.</div></div><div><h3>Conclusion</h3><div>Maternal antibiotics during pregnancy increased long-term risk of childhood respiratory infection risk following a dose–response pattern, which was linked to newborn metabolomic alterations.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 960-969"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148349065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B-cell receptor ligation selectively inhibits IgE class switch recombination","authors":"Adam K. Wade-Vallance PhD,&nbsp;Zhiyong Yang PhD,&nbsp;Jeremy B. Libang BS,&nbsp;Ananya R. Krishnapura BA,&nbsp;James B. Jung PhD,&nbsp;Emily W. Matcham BA,&nbsp;Chung-An M. Wu MD,&nbsp;Marcus J. Robinson PhD,&nbsp;Christopher D.C. Allen PhD","doi":"10.1016/j.jaci.2026.04.032","DOIUrl":"10.1016/j.jaci.2026.04.032","url":null,"abstract":"<div><h3>Background</h3><div>Mechanisms that restrict class switch recombination (CSR) to IgE may limit the subsequent production of IgE antibodies in allergic diseases. A role for B-cell receptor (BCR) signaling in IgE regulation was revealed in mice and in cultured B cells with altered BCR signaling. While prior work has focused on BCR signaling in IgE-switched cells, BCR signaling also reportedly inhibits CSR.</div></div><div><h3>Objective</h3><div>We sought to determine whether BCR signaling selectively inhibits IgE CSR.</div></div><div><h3>Methods</h3><div>We assessed whether BCR signaling strength affected IgE responses in immunized mice. For mechanistic evaluation, primary mouse or human B cells were induced to switch to IgE in cell culture and were perturbed with antibodies or cognate antigen to ligate the BCR, pharmacologic inhibitors of signaling proteins, and/or additional cytokines. Primary readouts were flow cytometry and RNA analysis.</div></div><div><h3>Results</h3><div>In immunized mice, BCR signaling strength inversely correlated with the relative frequencies of IgE-switched germinal center B cells and plasma cells. In mouse B-cell cultures, BCR signaling selectively inhibited IgE CSR in a manner dependent on ligand concentration, affinity, and avidity. This inhibition required Syk, whereas blockade of the PI3K subunit p110δ increased IgE cell frequencies independently of BCR ligation. The cytokines IL-21 or TGF-β1, in combination with BCR ligation, cooperatively inhibited IgE CSR. Similar results were observed in cultures of human tonsillar B cells.</div></div><div><h3>Conclusion</h3><div>IgE CSR is uniquely susceptible to inhibition by BCR signaling in mouse and human B cells, with important implications for the regulation and pathogenesis of allergic disease.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 1085-1100.e12"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and transcriptomic characterization of mixed granulocytic phenotype in chronic obstructive pulmonary disease","authors":"Clarus Leung MD,&nbsp;Jung-Wan Yoo MD, PhD,&nbsp;Hye Yun Park MD, PhD,&nbsp;Haad Bhutta BSc,&nbsp;Puneet Sidhu BASc,&nbsp;Elizabeth Guinto PhD,&nbsp;Graeme J. Koelwyn PhD,&nbsp;Milad Vahedi DVSc,&nbsp;Xuan Li MSc,&nbsp;Rachel L. Eddy PhD,&nbsp;Jonathon A. Leipsic MD,&nbsp;Fernando Sergio Leitao Filho MD,&nbsp;Julia S. Yang MSc,&nbsp;Stephen Milne PhD,&nbsp;Hiroto Takiguchi MD,&nbsp;Kentaro Akata MD,&nbsp;Seung Won Ra MD,&nbsp;Ji-Yong Moon MD, PhD,&nbsp;Hyun Kuk Kim MD,&nbsp;Yuji Cho MD,&nbsp;Don D. Sin MD","doi":"10.1016/j.jaci.2026.06.013","DOIUrl":"10.1016/j.jaci.2026.06.013","url":null,"abstract":"<div><h3>Background</h3><div>In chronic obstructive pulmonary disease (COPD), patients with peripheral airways infiltrated by eosinophils and neutrophils (“mixed granulocytic COPD”) show worse outcomes than those without.</div></div><div><h3>Objectives</h3><div>We sought to examine the expression of immune response and lung tissue remodeling pathways in patients with mixed granulocytic COPD.</div></div><div><h3>Methods</h3><div>In this <em>post hoc</em> study of the DISARM (A Study to Investigate the Differential Effects of Inhaled Symbicort and Advair on Lung Microbiota) randomized controlled trial, mixed granulocytic COPD was defined by eosinophils &gt;1% and neutrophils &gt;3% of the total leukocyte count in bronchoalveolar lavage (BAL). We compared clinical outcomes of mixed granulocytic COPD with 2 other phenotypes (neutrophilic, pauci-granulocytic). We then examined canonical pathways using gene set enrichment analysis and expression of immune cell and tissue remodeling gene signatures in BAL across phenotypes.</div></div><div><h3>Results</h3><div>Among 54 patients, 33% had mixed granulocytic COPD. Patients with mixed granulocytic COPD had the lowest FEV₁, the most radiographic emphysema, and the highest annualized exacerbation rates. Cell pellets of BAL in mixed granulocytic COPD showed upregulated gene expression of type 1 (TNFA, IL6, and IFNG signaling) and type 2 (IL4/13 signaling) immune responses relative to the neutrophilic and pauci-granulocytic phenotypes. Mixed granulocytic COPD was marked by increased expression of gene signatures for natural killer cells, B cells, and CD4 and CD8 naive and memory/effector T cells. Mixed granulocytic COPD showed the highest expression of tissue remodeling processes, which significantly associated with lower FEV₁.</div></div><div><h3>Conclusions</h3><div>Mixed granulocytic COPD is marked by complex immune responses in the peripheral airways and is associated with increased tissue remodeling that associates with more severe airflow limitation.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 982-993"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epitope-specific IgE profiles are predictive of desensitization and remission in the IMPACT trial","authors":"Julie Wang MD,&nbsp;Samane Khoshbakht PhD,&nbsp;Kyung Won Lee PhD,&nbsp;Stacie M. Jones MD,&nbsp;Michelle F. Huffaker MD,&nbsp;Marshall Plaut MD,&nbsp;Lisa M. Wheatley MD,&nbsp;Carolyn H. Baloh MD,&nbsp;Mayte Suárez-Fariñas PhD,&nbsp;Hugh A. Sampson MD","doi":"10.1016/j.jaci.2026.07.008","DOIUrl":"10.1016/j.jaci.2026.07.008","url":null,"abstract":"<div><h3>Background</h3><div>Results from the IMPACT trial suggest that initiation of peanut oral immunotherapy (pnOIT) before age 4 years can increase chances of achieving desensitization and remission.</div></div><div><h3>Objective</h3><div>We assessed sequential (linear) epitope-specific (es)-IgE and es-IgG₄ profiles over the course of pnOIT to determine whether they could predict desensitization and remission outcomes.</div></div><div><h3>Methods</h3><div>Participants in the IMPACT trial (NCT03345160) were randomized to pnOIT or placebo for 134 weeks. Desensitization and remission end points were assessed by oral food challenges. There were 93 (96.9%) of 96 participants in the pnOIT group and 47 (94%) of 50 in the placebo group. Specific IgE and IgG₄ levels to peanut, component proteins, and 64 allergenic epitopes were measured. Machine learning was used to develop predictive models for desensitization and remission.</div></div><div><h3>Results</h3><div>PnOIT was associated with an overall decrease in sequential es-IgE and increase in es-IgG₄ levels. Younger subjects (&lt;2.3 years old) had lower baseline es-IgE binding and lower fold change in es-IgE and es-IgG₄ binding during pnOIT. Participants with desensitization had lower baseline es-IgE levels than those without desensitization. A machine learning model that included 9 es-IgE antibodies predicted remission with an overall performance as follows: accuracy 88.2%, area under the curve 88.2%, sensitivity 83.3%, and specificity 90.0%—comparable to, but not better than, models based on peanut IgE.</div></div><div><h3>Conclusions</h3><div>Baseline epitope IgE profiles can predict remission outcome for children undergoing pnOIT. Age and baseline peanut IgE remain important factors across models.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 1018-1031"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584431","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":"The SPRR2A-CSTA axis drives IL-17A–induced squamous metaplasia and steroid resistance in allergic rhinitis","authors":"Shaobing Xie MD, PhD,&nbsp;Xuan Yuan BS,&nbsp;Liyuan Liu BS,&nbsp;Maonan Wu BS,&nbsp;Wenjing Gu MD, PhD,&nbsp;Hua Zhang MD, PhD,&nbsp;Zhihai Xie MD, PhD,&nbsp;Weihong Jiang MD, PhD,&nbsp;Peisong Gao MD, PhD","doi":"10.1016/j.jaci.2026.05.024","DOIUrl":"10.1016/j.jaci.2026.05.024","url":null,"abstract":"<div><h3>Background</h3><div>Epithelial remodeling, particularly squamous metaplasia (SM), is a common but understudied epithelial alteration in refractory allergic rhinitis (AR). Its molecular drivers and contribution to steroid resistance remain unclear.</div></div><div><h3>Objective</h3><div>We sought to define the epithelial keratinization program underlying SM in AR and determine its role in glucocorticoid resistance.</div></div><div><h3>Methods</h3><div>Nasal mucosa tissues from patients with refractory AR with or without SM were assessed by immunostaining and transcriptomic profiling. Small proline-rich protein 2A (SPRR2A)-deficient mice were used to determine the role of SPRR2A in epithelial keratinization and steroid responsiveness. Primary nasal epithelial cells were stimulated with IL-17A or cystatin A (CSTA) to evaluate SPRR2A-dependent keratinization and steroid resistance. Serum SPRR2A and CSTA levels were quantified in patients with AR stratified by steroid responsiveness.</div></div><div><h3>Results</h3><div>Transcriptomic analysis identified SPRR2A as a leading epithelial marker associated with SM in AR. SPRR2A-associated keratin remodeling, including upregulation of KRT6A and KRT13, represented a defining molecular signature of SM. Glucocorticoid receptor β, a key mediator of steroid resistance, was markedly increased and colocalized with KRT6A and KRT13 in SM tissues. IL-17A induced a robust SPRR2A-keratin remodeling module, generating a steroid-resistant epithelial state. Genetic deletion of Sprr2a abolished IL-17A–driven keratinization, prevented SM, and restored steroid responsiveness. Mechanistically, CSTA emerged as a SPRR2A-dependent effector that promoted squamous differentiation and epithelial GRβ induction. Csta-treated primary cultures recapitulated SM and conferred steroid resistance. Clinically, elevated serum SPRR2A and CSTA levels distinguished patients with steroid-resistant AR from those with steroid-responsive AR.</div></div><div><h3>Conclusions</h3><div>SPRR2A promotes epithelial SM and steroid resistance through CSTA, identifying the SPRR2A-CSTA axis as a potential therapeutic target and biomarker pathway in refractory AR.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 994-1009.e8"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217885","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":"Use of electronic cigarettes and asthma across the lifespan","authors":"Kimberly Pereira MD,&nbsp;Franziska Rosser MD, MPH,&nbsp;Yueh-Ying Han PhD,&nbsp;Ilona Jaspers PhD,&nbsp;Laura E. Crotty Alexander MD,&nbsp;Juan C. Celedón MD, DrPH, FAAAAI","doi":"10.1016/j.jaci.2026.07.009","DOIUrl":"10.1016/j.jaci.2026.07.009","url":null,"abstract":"<div><div>In the last 15 years, the tobacco industry has marketed electronic cigarettes (e-cigarettes) as a tool to help adults to quit cigarette smoking while also promoting their use in children and adolescents. As expected, this led to a marked increase in e-cigarette use (also called vaping) among children and adolescents in the United States. Although the prevalence of vaping decreased after the 2019 e-cigarette or vaping product use–associated lung injury epidemic and stricter regulations fueled by concurrent adoption of cigarette and marijuana smoking in youths, approximately 10% of middle- and high-school students in the United States report vaping. A growing body of experimental and epidemiologic evidence has implicated e-cigarette use in the pathogenesis of respiratory diseases such as chronic obstructive pulmonary disease, lung cancer, interstitial lung disease, and asthma. In this narrative review, we first evaluate the types and composition of e-cigarettes and trends in e-cigarette use and then assess findings from experimental and epidemiologic studies of e-cigarette exposure and asthma published to date. We end by discussing future directions for research in this field while emphasizing the need for prevention of and screening for e-cigarette use in youths and adults, particularly those affected with asthma.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 927-943"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Editors’ Choice","authors":"","doi":"10.1016/j.jaci.2026.08.013","DOIUrl":"10.1016/j.jaci.2026.08.013","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"158 4","pages":"Pages 944-948"},"PeriodicalIF":11.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149095606","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}