Journal of Allergy and Clinical Immunology最新文献

{"title":"Resolution of epithelial dysfunction in eosinophilic esophagitis is mediated by an HIF-1α-CD73-adenosine signaling axis","authors":"Shauna K. Kellett MSc ,&nbsp;Taylor Crue MPH ,&nbsp;Sofia N. Almeida Cruz MSc ,&nbsp;Gary E. Markey PhD ,&nbsp;Sinéad Ryan PhD ,&nbsp;Louise Crowe PhD ,&nbsp;Olga Fagan BSc, BM, BS ,&nbsp;Niall Conlon PhD, FRCPath ,&nbsp;Claire L. Donohoe MB BCh, BAO, BA, MMEd, PhD, FRCSI ,&nbsp;Susan McKiernan MB BCh, BAO ,&nbsp;Glenn T. Furuta MD ,&nbsp;Joanne C. Masterson PhD","doi":"10.1016/j.jaci.2025.09.006","DOIUrl":"10.1016/j.jaci.2025.09.006","url":null,"abstract":"<div><h3>Background</h3><div>Inflammatory hypoxia is induced by eosinophilic inflammation, while a decreased expression in the key hypoxic regulator, hypoxia-inducible transcription factor (hypoxia-inducible factor-1alpha [HIF-1α]), has been shown in patients with eosinophilic esophagitis (EoE), contributing to maladaptive hypoxic responses in the esophageal epithelium. Recent publications have reported attenuated CD73/ecto-5'-nucleotidase expression in patients with EoE, which is a known extracellular adenosine producing ecto-enzyme and a direct HIF-1α target.</div></div><div><h3>Objectives</h3><div>We sought to check the hypothesis that dysregulated CD73 facilitated epithelial wound healing and barrier dysfunction in EoE and was modulated by HIF-1α and mediated through impaired extracellular adenosine signaling.</div></div><div><h3>Methods</h3><div><em>In vitro</em> scratch assays and 3-dimensional air-liquid interface cultures were carried out on EPC2-hTERT cells to evaluate wound healing and barrier responses in the esophageal epithelium. Pharmacological CD73 inhibition (α,β-methylene adenosine-5-diphosphate), adenosine receptor A2B (ADORA2B) activation (BAY60-6583), and HIF-1α stabilization (dimethyloxalylglycine) were also used. <em>In vivo</em>, the L2-IL5^OXA, an HIF-1α overexpressing L2-IL5^OXA (<em>L2-IL5</em>^<em>+</em><em>/HIF-1A-dPA</em>^<em>+/+</em><em>/K14Cre</em>^<em>+</em>)^OXA, and ADORA2B agonist-BAY60-6583 (L2-IL5^OXABAY) EoE mouse models were used.</div></div><div><h3>Results</h3><div>Pharmacologic studies demonstrated that CD73 inhibition resulted in defective wound healing responses in scratch assays and decreased epithelial barrier in 3-dimensional air-liquid interface cultures. Activation of downstream ADORA2B signaling improved wound healing responses and barrier functions via restoration of fibronectin (<em>FN1</em>) and occludin (<em>OCLN</em>) expression. <em>In vivo</em> studies in L2-IL5^OXA EoE mouse models recapitulated <em>in vitro</em> findings of improved epithelial barrier integrity characterized by increased expression of occludin following ADORA2B agonism and HIF-1α stabilization.</div></div><div><h3>Conclusions</h3><div>Overall, our study suggests that defective HIF-1α signaling in extended hypoxia is a key driver of CD73 downregulation in EoE, leading to impaired extracellular adenosine signaling, defective wound healing, and barrier dysfunction, establishing the possibility for ADORA2B agonism as a potential novel therapeutic approach for EoE.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 693-710.e1"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103285","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":"Utilization of the All of Us Research Program in a study of genetics in Yao syndrome","authors":"Song Wu PhD ,&nbsp;Zuoming Deng PhD ,&nbsp;Asif Uddin MD ,&nbsp;Baozhong Xin PhD ,&nbsp;Peter D. Gorevic MD ,&nbsp;Qingping Yao MD, PhD","doi":"10.1016/j.jaci.2025.10.028","DOIUrl":"10.1016/j.jaci.2025.10.028","url":null,"abstract":"<div><h3>Background</h3><div>Yao syndrome (OMIM <span><span>617321</span><svg><path></path></svg></span>) is a chronic and recurring inflammatory disease linked to specific variants in the nucleotide-binding oligomerization domain containing protein 2 <em>(NOD2)</em> gene.</div></div><div><h3>Objective</h3><div>This study aimed to further dissect the genetic mechanisms of the disease.</div></div><div><h3>Methods</h3><div>A total of 405 patients suspected of having systemic autoinflammatory diseases were included. Molecular testing was performed using an autoinflammatory disease gene panel to aid diagnosis. To compare the frequencies of commonly encountered individual and combined <em>NOD2</em> variants, whole genome sequencing data from the All of Us Research Program, consisting of 128,196 participants of European ancestry, was interrogated.</div></div><div><h3>Results</h3><div>Commonly encountered <em>NOD2</em> variants and combinations were compared to the All of Us Research Program genomic data. We found that <em>NOD2</em> variant IVS8 + 158 (JW1) was significantly more prevalent in the patient population (odds ratio [OR] = 1.32, <em>P</em> = .006). Similarly, <em>NOD2</em> variants p.Leu1007Profs∗2 and p.Arg703Cys were significantly higher in the patient population (OR = 1.61, <em>P</em> = .018; OR = 2.66, <em>P</em> = .004, respectively). Linkage disequilibrium analysis demonstrated a haplotype configuration for IVS8 + 158 and p.Arg702Trp or IVS8 + 158 (JW1) and p.Leu1007Profs∗2. Additionally, <em>NOD2</em> IVS8 + 158 (JW1) and p.Val955Ile was found to be significantly more frequent in the patient group (OR = 1.63, <em>P</em> = .038). These findings confirm and further expand the association of these individual and combined <em>NOD2</em> variants with Yao syndrome.</div></div><div><h3>Conclusion</h3><div>This large case–control study of population genetics provides valuable insights into the genetic mechanisms of Yao syndrome and has important implications for ordering genetic tests, interpretation of the results, genomic diagnosis, and genetic counseling.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 767-775"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145461950","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":"Caution in interpreting MRGPRX2 N62S as a disease-driving variant in chronic spontaneous urticaria","authors":"Margarita Martín PhD ,&nbsp;Paola Leonor Quan MD ,&nbsp;Laia Ollé PhD ,&nbsp;Marina Sabaté-Bresco PhD ,&nbsp;Gabriel Gastaminza MD, PhD","doi":"10.1016/j.jaci.2025.11.013","DOIUrl":"10.1016/j.jaci.2025.11.013","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Page 781"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849502","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":"Biologics in the treatment of severe asthma in children and adults—updates 2024-2025","authors":"Courtney L. Gaberino MD ,&nbsp;Jason Moraczewski MD ,&nbsp;Daniel J. Jackson MD ,&nbsp;Leonard B. Bacharier MD","doi":"10.1016/j.jaci.2026.01.002","DOIUrl":"10.1016/j.jaci.2026.01.002","url":null,"abstract":"<div><div>The development of targeted mAbs has transformed the treatment of moderate-to-severe asthma. The main clinical trial outcomes have focused on exacerbation reduction and lung function improvement. In the past few years, there have been many high-quality studies examining pathophysiologic effects of the biologic therapies, giving insight into their downstream impacts. Clinical remission is a growing area of interest, and many studies highlight the utility as well as the limitations of commonly available biomarkers to predict treatment response. This review synthesizes the results of recent clinical trials and related topics focusing on relevant updates to the literature since 2024, highlighting new indications for use, predictors of response, safety data, real-world comparative effectiveness, remission, and mechanistic advances.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 575-587"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014523","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":"Staphylococcus aureus in atopic dermatitis: How a common bacterium exploits and drives disease","authors":"Carla Chehadeh BS ,&nbsp;Teruaki Nakatsuji PhD ,&nbsp;Richard L. Gallo MD, PhD","doi":"10.1016/j.jaci.2025.12.1009","DOIUrl":"10.1016/j.jaci.2025.12.1009","url":null,"abstract":"<div><div>The role of <em>Staphylococcus aureus</em> in atopic dermatitis (AD) has been extensively studied. Although its role in the pathophysiology of AD was previously controversial, current evidence now shows that it is a major factor promoting the disease and is responsible for significant morbidity. Its influence in AD stems from widespread exposure because <em>S aureus</em> is common on healthy skin and is frequently part of the normal human skin microbiome. In AD, <em>S aureus</em> and the closely related <em>Staphylococcus epidermidis</em> gain a selective growth advantage over most other members of the skin microbiome due to a complex relationship involving the skin’s innate immune system, other members of the microbiome, and skin barrier properties. Disruption in the functioning of these components or changes in their interactions lead to dysbiosis, skin barrier damage, and the progression of skin disease. This review summarizes research findings on these relationships and highlights the interactions and factors that promote <em>S aureus</em> survival on skin and its participation in the pathogenesis of AD.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 551-557"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962092","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":"A Special Thank-You to Our Reviewers","authors":"","doi":"10.1016/S0091-6749(26)00064-3","DOIUrl":"10.1016/S0091-6749(26)00064-3","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 588-591"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147334356","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":"Neutralizing IL-22RA1 improves histologic and molecular alterations associated with atopic dermatitis pathogenesis","authors":"Sophia Wasserer MD ,&nbsp;Thomas Litman PhD ,&nbsp;Josephine Hebsgaard PhD ,&nbsp;Manja Jargosch PhD ,&nbsp;Christina Hillig MSc ,&nbsp;Anna Caroline Pilz MD ,&nbsp;Natalie Garzorz-Stark MD, PhD ,&nbsp;Tilo Biedermann MD ,&nbsp;Christophe Blanchetot PhD ,&nbsp;Michael Menden PhD ,&nbsp;Mette Sidsel Mortensen MSc ,&nbsp;Tine Skak-Nielsen PhD ,&nbsp;Malene Bertelsen PhD ,&nbsp;Birgitte Ursoe PhD ,&nbsp;Felix Lauffer MD, PhD ,&nbsp;Britta C. Martel PhD ,&nbsp;Kilian Eyerich MD, PhD ,&nbsp;Stefanie Eyerich PhD","doi":"10.1016/j.jaci.2025.08.033","DOIUrl":"10.1016/j.jaci.2025.08.033","url":null,"abstract":"<div><h3>Background</h3><div>Disease of a subgroup of patients with atopic dermatitis (AD) does not show sufficient improvement with current systemic therapies, highlighting the heterogeneity of the chronic inflammatory skin disease and the need for novel treatments.</div></div><div><h3>Objective</h3><div>In this study, we investigated the pathogenic contribution of the IL-22/IL-22 receptor (IL-22RA1) axis to AD skin inflammation in <em>in vitro, ex vivo,</em> and <em>in vivo</em> models to evaluate the therapeutic potential of blocking this axis.</div></div><div><h3>Methods</h3><div><em>IL</em><em>22RA1</em> expression in AD skin was assessed by <em>in situ</em> hybridization. Inhibition of the IL-22/IL-22R signaling cascade was evaluated in a human AD <em>in vitro</em> model (3-D skin equivalents) and a phorbol 12-myristate 13-acetate (aka TPA) mouse model using temtokibart, a humanized antibody directed against IL-22RA1.</div></div><div><h3>Results</h3><div><em>IL22RA1</em> was highly expressed in the epidermis of lesional AD skin versus nonlesional control skin; expression correlated positively with epidermal thickness and negatively with the barrier integrity marker loricrin. IL-22 stimulation in 3-D skin equivalents induced a specific molecular signature associated with lack of terminal differentiation, altered lipid metabolism, and increased immune response. Inhibition of IL-22RA1 with temtokibart showed significant improvements in skin barrier integrity at the histologic and molecular levels. IL-22RA1 inhibition in a skin inflammation mouse model with Zymo, a surrogate murine anti–IL-22RA1 monoclonal antibody for temtokibart, reduced local expression of Cxcl1 and <em>S100a9</em>.</div></div><div><h3>Conclusions</h3><div>These findings suggest that the IL-22/IL-22RA1 axis functionally contributes to AD pathogenesis. Thus, blocking IL-22RA1 represents a potentially valuable new therapeutic option.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 653-665"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498678","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":"Autonomic dysfunction and vasoregulation in long COVID-19 are linked to anti-GPCR autoantibodies","authors":"Boris Schmitz PhD ,&nbsp;René Garbsch PhD ,&nbsp;Hendrik Schäfer MSc ,&nbsp;Christian Bär PhD ,&nbsp;Shambhabi Chatterjee PhD ,&nbsp;Gabriela Riemekasten MD ,&nbsp;Kai Schulze-Forster PhD ,&nbsp;Harald Heidecke PhD ,&nbsp;Christoph Schultheiß PhD ,&nbsp;Mascha Binder MD ,&nbsp;Frank C. Mooren MD","doi":"10.1016/j.jaci.2025.10.034","DOIUrl":"10.1016/j.jaci.2025.10.034","url":null,"abstract":"<div><h3>Background</h3><div>Severe acute respiratory syndrome coronavirus 2–triggered autoantibodies (AABs) targeting G protein–coupled receptors have been suggested to contribute to the post–acute sequelae of coronavirus disease 2019 (or post–COVID-19 syndrome [PCS]).</div></div><div><h3>Objective</h3><div>We sought to characterize AABs involved in autonomic dysfunction such as rhythm control and vasoregulation in patients with PCS and profile the peripheral B- and T-cell receptor (BCR/TCR) architecture to identify immunogenetic imprints of autoimmunity.</div></div><div><h3>Methods</h3><div>Anti–G protein–coupled receptor AABs were characterized in patients with PCS with known alteration in autonomic nervous system functions assessed by heart rate variability. Adaptive immune receptor repertoire sequencing was used to profile peripheral BCR and TCR architecture. Patients with COVID-19 with severe or moderate acute disease, after recovery, and prepandemic healthy individuals served as controls. Cardio- and vasoactive effects of AABs were analyzed using 24-hour and exercise test blood pressure measurements. The direct effect of AABs on electromechanical coupling was tested in human-induced pluripotent stem cell cardiomyocytes.</div></div><div><h3>Results</h3><div>AABs including autoantibody against angiotensin II receptor type 1/2, autoantibody against adrenoceptor beta 1/2, autoantibody against muscarinic acetylcholine receptor M1/M3, and autoantibody against C-X-C motif chemokine receptor 3 (CXCR3ab) were associated with heart rate variability alterations. Analysis of the broad BCR repertoire metrics revealed high similarity between patients with PCS and healthy controls for clonality and diversity measures. The level of somatic hypermutation as proxy for antigen experience was equal to that of healthy controls. Elevated CXCR3ab levels were linked to higher 24-hour mean arterial pressure, whereas patients with elevated autoantibody against muscarinic acetylcholine receptor M1 and CXCR3ab levels showed higher blood pressure during stress tests. AABs had no effect on beat frequency and amplitude of cardiomyocyte contraction <em>in vitro</em>.</div></div><div><h3>Conclusions</h3><div>These findings suggest that AABs play a modulatory role in sympathetic nervous system–mediated regulation of cardiac rhythm and vascular function in PCS. AAB levels did not correlate with BCR and TCR repertoire metrics or T-cell receptor beta variable gene usage.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 722-738.e7"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145559944","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":"News beyond our pages","authors":"","doi":"10.1016/j.jaci.2026.01.003","DOIUrl":"10.1016/j.jaci.2026.01.003","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 597-598"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147334357","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":"NOX2 deficiency enhances priming and activation of the NLRP3 inflammasome","authors":"Blandine Monjarret MSc ,&nbsp;Sara Shour MSc ,&nbsp;Daniela Stanga PhD ,&nbsp;Aissa Benyoucef PhD ,&nbsp;Emilie Heckel PhD ,&nbsp;Lorie Marchitto MSc ,&nbsp;Jennifer W. Leiding MD ,&nbsp;Guilhem Cros MD ,&nbsp;Isabel Fernandez PhD ,&nbsp;Jean-Sebastien Joyal MD, PhD ,&nbsp;Fabien Touzot MD, PhD","doi":"10.1016/j.jaci.2023.09.030","DOIUrl":"10.1016/j.jaci.2023.09.030","url":null,"abstract":"<div><h3>Background</h3><div><span><span>Nicotinamide adenine dinucleotide phosphate </span>oxidase<span> complex 2 (NOX2) deficiency, or chronic granulomatous disease<span> (CGD), is an inborn error of immunity associated with increased susceptibility to infection and inflammatory manifestations. The pathophysiologic mechanism leading to the increased </span></span></span>inflammatory response in CGD remains elusive.</div></div><div><h3>Objective</h3><div><span><span>We investigated the pathophysiologic mechanisms leading to NOD-like receptor family pyrin domain containing 3 (NLRP3) </span>inflammasome activation in </span>NOX2 deficiency.</div></div><div><h3>Methods</h3><div><span>We used NOX2-deficient human primary and CRISPR-engineered macrophages to show that NOX2 deficiency enhances the inflammatory response mainly by modulating the 2 steps of NLRP3 </span>inflammasome activation: its transcriptional priming and its posttranslational triggering.</div></div><div><h3>Results</h3><div><span>At the transcriptional level, NOX2-deficient phagocytes<span><span> display increased priming of the NLRP3 inflammasome, as evidenced by increased transcription of NLRP3 and IL-1β through an IL-1β–dependent stimulation of the nuclear factor kappa–light-chain enhancer of activated B cells (aka NF-κB) pathway. At the posttranslational level, the </span>absence of NOX2 triggers the NLRP3 inflammasome activation by increased K</span></span>⁺<span> efflux and excessive release of mitochondrial DNA due to mitochondrial damage. Furthermore, NLRP3-driven pyroptosis<span> in NOX2-deficient phagocytes further enhances NLRP3 activation by increasing K</span></span>⁺ efflux.</div></div><div><h3>Conclusion</h3><div>Our results unveil the role of NOX2 as a repressor of the inflammatory response at both transcriptional and posttranslational levels and pave the way for a more targeted approach to treating CGD patients with inflammatory manifestations.</div></div>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":"157 3","pages":"Pages 711-721.e5"},"PeriodicalIF":11.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41133435","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}