Clinical Reviews in Allergy & Immunology最新文献

{"title":"Extracellular Vesicles in Allergy: From Cellular Communication to Clinical Implications.","authors":"Angelika Sysak, Sabina Górska","doi":"10.1007/s12016-026-09161-7","DOIUrl":"10.1007/s12016-026-09161-7","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are lipid bilayer-enclosed particles released by both eukaryotic and prokaryotic cells and represent an evolutionarily conserved system of intercellular communication. By transporting bioactive cargo, including proteins, lipids, microRNAs, EVs enable the transfer of molecular signals between cells, thereby regulating immune homeostasis and inflammatory responses. In allergic diseases, EVs have emerged as key mediators linking epithelial barriers, immune cells, and the microbiome. EVs derived from epithelial, immune, and microbiota-associated cells may contribute to the initiation, amplification, and persistence of allergic inflammation by modulating barrier integrity, immune cell polarization, and cytokine signaling pathways. Disease-specific alterations in EV cargo reflect underlying pathogenic mechanisms, positioning EVs as promising non-invasive biomarkers for disease diagnosis, stratification, and monitoring. In parallel, accumulating experimental evidence highlights the therapeutic potential of EVs as cell-free immunomodulatory agents capable of suppressing allergic inflammation and promoting immune tolerance. This review synthesizes current knowledge on extracellular vesicles across three major allergic diseases: asthma, atopic dermatitis, and food allergy, integrating mechanistic insights with diagnostic and therapeutic advances. By incorporating highly recent literature and covering a broad spectrum of EV sources and engineered vesicle-based strategies, the review provides a comprehensive overview of how EV-mediated cellular communication translates into clinically relevant applications in allergy.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Update Comprehensive Review on Epigenetic Modifications and Therapies in Autoimmune Diseases.","authors":"Hui Chen, Suqing Zhou, Fanghan Ji, Kaili Chen, Lian Jian, Yiming Wang, Hongmei Yao, Ming Yang, Haijing Wu","doi":"10.1007/s12016-026-09133-x","DOIUrl":"10.1007/s12016-026-09133-x","url":null,"abstract":"<p><p>Autoimmune diseases are chronic disorders characterized by dysregulated immune responses directed against self-tissues. However, current therapies are limited by suboptimal efficacy, substantial adverse effects, or an inability to halt or reverse disease progression. Emerging evidence indicates that epigenetic regulation—including DNA methylation, histone modification and non-coding RNA—has a central role in the pathogenesis of autoimmune diseases, creating transformative opportunities for the development of targeted therapies. This review provides an up-to-date synthesis of advances in epigenetic drugs for major autoimmune diseases including systemic lupus erythematosus and rheumatoid arthritis, and examines the molecular mechanisms through which these agents modulate immune cell differentiation and function. Accumulating data from preclinical models and clinical studies suggest that epigenetic therapies not only suppress inflammation but also reprogramme aberrant immune states, conferring therapeutic potential for disease amelioration. At present, twelve epigenetic drugs have been approved for cancer, and given the shared epigenetic abnormalities between cancer and autoimmune diseases, extending these therapeutic indications to autoimmune disorders represents a feasible strategy. Moreover, combination regimens incorporating epigenetic drugs have demonstrated enhanced therapeutic efficacy. These findings highlight opportunities for drug repurposing and translational innovation. Despite challenges related to specificity and safety, epigenetic therapies are poised to drive a paradigm shift in the treatment of autoimmune diseases, and future studies integrating epigenomic profiling with precision medicine will be essential to enable their personalised clinical application.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Features, Diagnosis, and Treatment of Eosinophilic Sialodochitis: A Systematic Review of the Literature.","authors":"Alvaro Sánchez Barrueco, William Aragonés Sanzen-Baker, Marta Santiago Horcajada, Pilar Benavent Marín, Gonzalo Díaz Tapia, Jessica Mireya Santillán Coello, Virginia Ruiz San José, Christian Calvo-Henríquez, Carlos Cenjor Español, José Miguel Villacampa Aubá","doi":"10.1007/s12016-026-09160-8","DOIUrl":"10.1007/s12016-026-09160-8","url":null,"abstract":"<p><p>Eosinophilic sialodochitis is an under-recognized obstructive inflammatory disorder of the major salivary ducts that has been described under heterogeneous terms, including allergic parotitis, fibrinous sialodochitis, and Kussmaul disease. We systematically reviewed the literature to summarize nomenclature, clinical presentation, diagnostic assessment, treatment, and consistency with proposed diagnostic criteria. We searched six bibliographic databases from inception to December 2025, complemented by Google Scholar and citation tracking. Studies describing eosinophilic sialodochitis or related entities were included irrespective of language. Data were synthesized descriptively because of marked heterogeneity. Seventy-nine studies involving 387 patients were included, comprising 64 full-text reports and 15 conference abstracts or posters. Most publications were case reports or case series. Recurrent parotid and/or submandibular swelling, eosinophil-rich salivary mucus plugs, ductal dilatation or stenosis, and frequent atopic comorbidity were the most characteristic findings. Eosinophils were identified in salivary mucus in 53 of 58 studies reporting local samples. Full compliance with published diagnostic criteria varied markedly, from 45 of 79 studies using the Baer framework to 2 of 79 using the Carey framework, while no study fully satisfied the Zhao framework. Treatment was usually multimodal and included antihistamines, corticosteroids, intraductal irrigation, sialendoscopy-assisted procedures, and, in selected refractory cases, biologic agents targeting type 2 inflammation. The available evidence supports eosinophilic sialodochitis as a distinct but incompletely standardized clinicopathological entity. Interpretation is limited by heterogeneity, incomplete reporting, and low-certainty evidence. Standardized definitions and minimum reporting items are needed to improve diagnostic certainty and comparability.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Evolving Landscape of CAR T-Cell Therapy in Autoimmune Diseases: A State-of-the-Art Review (2025).","authors":"Changpei Li, Hongjiang Liu, Shuyi Liao, Yifan Wang, Geng Yin, Qibing Xie","doi":"10.1007/s12016-026-09151-9","DOIUrl":"10.1007/s12016-026-09151-9","url":null,"abstract":"<p><p>Autoimmune diseases, characterized by a breakdown in immune tolerance and persistent autoantibody production, have traditionally been managed primarily through broad-spectrum immunosuppression. Chimeric antigen receptor (CAR) T-cell therapy, a groundbreaking modality once exclusive to oncology, has recently emerged as a transformative approach for treating autoimmunity. We conducted a comprehensive review and investigation into the applications of CAR T-cell therapy in distinct autoimmune diseases, mainly rheumatic diseases, exploring the full spectrum of CAR T modalities, including autologous, allogeneic, and the latest in vivo CAR T strategies. By combining preclinical studies with clinical evidence, we aim to elucidate the substantial potential of CAR T cells to achieve drug-free remission in autoimmune disorders through deep depletion of B cells and immune reset. Despite these promising outcomes from small cohorts or case studies, significant hurdles remain in the realms of safety and toxicity management, economic burden, complex manufacturing processes, and accessibility. In summary, this cross-disease and cross-platform review has thoroughly examined the current state of CAR T-cell therapy research for autoimmune diseases up to December 2025, providing updated insights and future perspectives on this transformative therapeutic strategy.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis as a Pathogenic Mechanism and Therapeutic Target in Autoimmune and Inflammatory Skin Diseases.","authors":"Peilong Guo, Fangqi Chen, Ming Zhao","doi":"10.1007/s12016-025-09125-3","DOIUrl":"10.1007/s12016-025-09125-3","url":null,"abstract":"<p><p>Ferroptosis represents an iron-dependent cell death pathway driven by lipid peroxide accumulation. Recent research has established that ferroptosis is closely linked to the pathogenesis and progression of various autoimmune and inflammatory skin diseases. This article systematically reviews the biological basis of ferroptosis and its specific regulatory characteristics in the skin, focusing on three core mechanisms: iron metabolism, lipid metabolism, and redox homeostasis. It emphasizes the hierarchical, dynamic, and complex nature of the skin, as a barrier organ exposed to the external environment, in maintaining ferroptosis homeostasis. This article focuses on representative diseases such as psoriasis, systemic lupus erythematosus, vitiligo, systemic sclerosis, photodermatoses, and atopic dermatitis. It summarizes the mechanisms by which ferroptosis is involved in skin cell injury, immune activation, inflammation maintenance, and autoantigen exposure. Finally, considering the current research limitations and gaps, the article proposes the potential of ferroptosis as a therapeutic target for autoimmune and inflammatory skin diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enzyme-Crosslinked House Dust Mite Exhibits Reduced Allergenic Activity by Reprogramming the AMPKα-RALDH2 Axis in Type 1 Dendritic Cells.","authors":"Tingting Zheng, Ishfaq Ahmed, Jiaqi Deng, Jiawen Shang, Yutong Yang, Wanjuan Zhong, Luwen Zhang, Weibin Jiang, Yangjie Zeng, Caimei Song, Yanyan Wang, Suidong Ouyang, Meng Yang, Xinguang Liu, Lei Wu, Jinlyu Sun, Gonghua Huang","doi":"10.1007/s12016-026-09159-1","DOIUrl":"10.1007/s12016-026-09159-1","url":null,"abstract":"<p><p>Enzymatic crosslinking has emerged as an effective strategy to reduce allergenicity, but the underlying immunological mechanisms involved remain largely unknown. Here we developed a hypoallergenic house dust mite (HDM) product, termed Tyr-HDM, by tyrosinase/caffeic acid–mediated crosslinking combined with galactomannan conjugation. Compared with control HDM, Tyr-HDM exhibited significantly reduced allergenic activity in a murine model of allergic asthma, as evidenced by attenuated airway inflammation and diminished T helper 2 (Th2) responses, including reduced IL-4, IL-5 and IL-13 production, accompanied by a notable increase in regulatory T (Treg) cells. Further mechanistic analysis revealed that Tyr-HDM modulated the Treg/Th2 balance through activation of the AMPKα−RALDH2 signaling axis specifically within type 1 conventional dendritic cells (cDC1s). Importantly, pharmacological inhibition of AMPK activity abolished the Tyr-HDM–induced Treg/Th2 reprogramming and the associated attenuation of allergic inflammation. In contrast, AMPK activation in cDC1s alleviated HDM−induced allergic inflammation. Notably, Tyr-HDM exerted both protective and therapeutic efficacy in HDM-driven allergic airway inflammation. Collectively, these findings demonstrate that enzymatically crosslinked HDM possesses reduced allergenic activity and distinct immunomodulatory properties and identify the AMPKα−RALDH2 axis in cDC1s as a key pathway linking allergen modification to immune regulation in allergic airway inflammation.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sexual Dimorphism in Allergic and Mast Cell-Associated Diseases.","authors":"Aditya Kotha, Tania D Maldonado, Hadi Hamze, Zakaria Y Hussain, Navya Gobinathan, An Z Yao, Mahamed Abudulkadir, John M Ching, John J Ryan","doi":"10.1007/s12016-026-09150-w","DOIUrl":"10.1007/s12016-026-09150-w","url":null,"abstract":"<p><p>Allergic diseases are common, affecting more than one-third of the global population and varying widely in severity. A consistent theme in asthma, food allergy, atopic dermatitis, and chronic urticaria is a female-dominant prevalence in adulthood. Some of these begin with male predominance in childhood and shift with puberty. A smaller subset of allergic diseases, including eosinophilic esophagitis and vernal keratoconjunctivitis, has a clear male prevalence. In fact, nearly all allergic diseases exhibit sexual dimorphism in either prevalence or severity. These striking disparities are being unraveled to reveal mechanisms that might be clinically targeted. In this review, we discuss the current state of knowledge about sexual dimorphism for these important inflammatory disorders. These insights are foundational for optimizing personalized medicine.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13068717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Regnase-1 in Autoimmune Diseases - A Future Therapeutic Target for Clinical Use.","authors":"Minghui Wang, Zhanjun Huang, Xun Gong, Ke Rui, Jie Tian, Ming Liu","doi":"10.1007/s12016-026-09156-4","DOIUrl":"10.1007/s12016-026-09156-4","url":null,"abstract":"<p><p>Regnase-1, encoded by ZC3H12A gene, is a multifunctional immune regulator that maintains immune homeostasis through its RNase activity. By controlling mRNA stability, microRNA maturation, and ubiquitin-dependent signaling, Regnase-1 fine-tunes inflammatory responses in both innate and adaptive immune cells. Accumulating evidence has demonstrated that dysregulation of Regnase-1 contributes to aberrant immune activation and the development of autoimmune diseases. In this review, we summarize recent advances in understanding the molecular mechanisms underlying Regnase-1 function, including RNase-mediated degradation of proinflammatory transcripts, suppression of microRNA (miRNA) biogenesis, and deubiquitination of key signaling intermediates such as TNF receptor-associated factor (TRAF) family proteins. We further discuss the multilayered regulation of Regnase-1 expression at transcriptional, post-transcriptional, and post-translational levels, highlighting how inflammatory cues dynamically modulate its activity. Importantly, Regnase-1 exerts cell type-specific functions among macrophages, neutrophils, T cells, B cells, and innate lymphoid cells, thereby modulating immune activation, differentiation, and effector responses. Recent studies have linked Regnase-1 to the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), multiple sclerosis (MS), psoriasis, and type 1 diabetes (T1D), suggesting its potential as a candidate biomarker or therapeutic target in autoimmune disorders. Regnase-1 has been shown to serve as a key negative regulator of inflammatory signaling pathways, including IL-23/IL-17–driven responses implicated in autoimmune pathogenesis. Although available data are largely derived from experimental models and observational clinical studies, current findings collectively highlight Regnase-1 as an upstream regulator of several inflammatory signaling pathways already being targeted in clinical practice. Further understanding of the disease- and cell-specific roles of Regnase-1 may facilitate the identification of novel diagnostic markers and the development of therapeutic targeting of Regnase-1 to restrain inflammatory response in autoimmune diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory B Cells at the Crossroads of Epigenetic Control and Immune Homeostasis.","authors":"Duminduni Hewa Angappulige, Darby J Ballard, Christina James Thomas, Shan Xu, Xinlei Guo, Yashvi Bhavin Gandhi, Sushim Mishra, Paul de Figueiredo, Jianxun Song","doi":"10.1007/s12016-026-09140-y","DOIUrl":"10.1007/s12016-026-09140-y","url":null,"abstract":"<p><p>Regulatory B cells (Bregs) cooperate with FOXP3⁺ regulatory T cells (Tregs) to maintain immune tolerance. Among diverse Breg subsets, IL-10⁺ Bregs are the best-defined mediators of suppression across autoimmunity and cancer. We synthesize evidence that histone deacetylases (HDACs) are the central epigenetic switch coupling cytokine and checkpoint signals to the Il10 locus, thereby programming Breg identity and stabilizing immunosuppression. Mechanistically, Blimp-1, STAT3, and c-Maf integrate environmental cues (e.g., LPS, IL-21, TIM-1 ligation) with HDAC-directed chromatin accessibility, while BACH2 and HDAC3 restrain Prdm1 to gate plasmablast-like Breg differentiation. We outline how this HDAC–IL-10 module coordinates Breg–Treg crosstalk (CD40/CD40L, PD-1/PD-L1, TIGIT, adenosinergic CD39/CD73) to suppress Th1/Th17 effectors. Disease context dictates outcome: Breg deficits fuel autoimmunity, whereas Breg expansion/reprogramming in tumors dampens cytotoxic immunity (PD-L1⁺, VISTA⁺, IL-35⁺ Bregs). We propose a framework for precision epigenetic modulation: enhancing HDAC-sensitive Breg programs to restore tolerance in autoimmunity, and disrupting tumor-skewed Breg circuits (PD-L1/VISTA, IL-35/STAT3, adenosine metabolism) to improve cancer immunotherapy. This perspective unifies Breg heterogeneity under a tractable axis—HDAC-tuned IL-10 chromatin—and highlights clinically actionable levers at the interface of epigenetics and immune regulation.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13061772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Biomarkers and Therapeutic Targets for Idiopathic Inflammatory Myopathies Related Lung Disease.","authors":"Hongzheng Wu, Xiaomeng Li, Honglin Xu, Zhixin Xu, Jingdi Zhang, Shulan Zhang, Yongzhe Li","doi":"10.1007/s12016-026-09157-3","DOIUrl":"10.1007/s12016-026-09157-3","url":null,"abstract":"<p><p>In adults with idiopathic inflammatory myopathies (IIM), interstitial lung disease (ILD) is a common and severe complication, particularly in those with anti-MDA5 antibody-positive dermatomyositis and antisynthetase syndrome. Notably, patients with rapidly progressive ILD associated with anti-MDA5 antibodies experience high rates of short-term mortality. As such, it is of paramount importance to identify effective blood-based biomarkers to predict disease occurrence, progression, and prognosis in this patient population, as they could facilitate early intervention, stratified management, and treatment adjustment. Beyond the well-established myositis-specific/associated autoantibodies for diagnosis, recent research has explored the predictive and prognostic value of serum biochemical markers, inflammatory cytokines, macrophage activation markers, specific immune cell subsets, and immune-related genetic signatures across different clinical courses of idiopathic inflammatory myopathy-associated ILD (IIM-ILD). Concurrently, pathogenesis-driven targeted therapies represent a promising avenue for refining current treatment strategies. Therefore, this review summarizes recent advances in blood-based biomarkers for IIM-ILD, exploring the underlying pathogenesis and their associated therapeutic targets, and highlighting possible challenges and future research directions in this field.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}