Clinical Reviews in Allergy & Immunology最新文献

{"title":"Management and Immunotherapy for Fungal Allergy: Clinical Practice and Unmet Needs.","authors":"Yongshi Yang, Yangxue Fu, Jinlyu Sun, Pascal Demoly, Rongfei Zhu","doi":"10.1007/s12016-026-09158-2","DOIUrl":"10.1007/s12016-026-09158-2","url":null,"abstract":"<p><p>Fungal allergy is an increasingly recognized health issue, affecting a notable proportion of the general population and a large majority of asthmatics, with sensitization rates rising globally. It contributes to a spectrum of respiratory diseases such as allergic rhinitis, allergic asthma, allergic fungal rhinosinusitis, and allergic bronchopulmonary aspergillosis, often associated with severe symptoms and poor disease control. Current management of fungal allergy relies on environmental control, pharmacotherapy, and allergen immunotherapy (AIT). However, AIT for fungal allergy remains limited by the lack of standardized, high-quality fungal extracts and low-certainty clinical evidence, despite promising results in small-sample trials, particularly for Alternaria alternata and Cladosporium herbarum. Recent advances in biologics targeting type 2 inflammation show promise for severe fungal-driven diseases. Key challenges include molecular allergy diagnosis, extract standardization, optimizing AIT strategies through novel formulations, and conducting large-scale randomized trials. Future progress hinges on collaborative efforts to develop precise diagnostics, improve therapeutic consistency, and validate combination approaches such as AIT with biologics. This review synthesizes current knowledge on the epidemiology, immunopathogenesis, and treatment of fungal allergy, highlighting the urgent needs and further clinical research to improve patient outcomes.</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":"147590430","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":"The Self-amplifying Inflammatory Cascade in Obstetric Antiphospholipid Syndrome: From Pathophysiology to Placenta-centric Immunotherapeutic Targets.","authors":"Rui Yan, Yuxin Wei, Lu Chen, Shaodan Zhu, Xudong Dong","doi":"10.1007/s12016-026-09153-7","DOIUrl":"10.1007/s12016-026-09153-7","url":null,"abstract":"<p><p>Obstetric Antiphospholipid Syndrome (OAPS) is an autoimmune-driven pregnancy complication whose core pathology is a dysregulated inflammatory cascade at the maternal-fetal interface, rather than the traditionally emphasized thrombosis. Antiphospholipid antibodies (aPL) trigger a diverse array of innate immune pathways, including the complement system, neutrophils, and the inflammasome, leading to trophoblast dysfunction, poor placentation, and ultimately, adverse pregnancy outcomes such as recurrent miscarriage, preeclampsia, and fetal growth restriction. The current standard of care, low-dose aspirin combined with heparin, primarily targets coagulation and has limited efficacy in controlling the underlying inflammatory response, resulting in treatment failure in approximately 20–30% of patients. This review aims to redefine the inflammatory nature of OAPS, elaborate on the immune-pathological network centered on the placenta, and critically examine the pivotal role of the signaling cascade mediated by TLR4 that activates the downstream NF-κB transcription factor as a major regulatory node of the inflammatory response. In this context, experimental inhibitors target the initiation of this cascade at the receptor level to prevent the subsequent nuclear translocation of NF-κB. Building on this, we review the evolution of treatment strategies from traditional anticoagulants to immunosuppressants and propose that “targeting the local placental immune microenvironment” is the core direction for future therapies. Finally, this paper discusses a novel snail-inspired bioactive substance, specifically focusing on the natural glycosaminoglycan AFG (Achatina fulica glycosaminoglycan). This glycosaminoglycan is a non-anticoagulant heparin-like GAG purified from snail mucus, characterized by a regular repeating sequence of →4)-β-D-GlcNAc(1→4)-α-L-IdoA2S(1→. AFG functions as a specialized immunomodulator that stabilizes placental cellular signaling by precisely targeting the placental inflammatory axis.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147580536","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":"Therapeutic Potential of Tulisokibart and Anti-TL1A Therapy in Inflammatory Disorders: Current Insights and Future Directions.","authors":"Juling Sia, Bernett Lee, Hazel H Oon","doi":"10.1007/s12016-026-09152-8","DOIUrl":"10.1007/s12016-026-09152-8","url":null,"abstract":"<p><p>Tumor necrosis factor-like cytokine 1 A (TL1A), encoded by the TNFSF15 gene, is expressed on multiple cells, including endothelial cells and dendritic cells, and in a soluble form in serum. Due to its central role in regulating immune response, TL1A has been implicated in the pathogenesis of several autoimmune inflammatory diseases such as inflammatory bowel disease (IBD), psoriasis and rheumatoid arthritis (RA). Mechanistically, TL1A exerts proinflammatory effects through binding of death receptor 3 (DR3) to activate downstream signalling cascades that drive inflammation and apoptosis. Tulisokibart, a novel humanized anti-TL1A monoclonal antibody, has garnered significant attention following phase 2 clinical trials demonstrating robust efficacy in IBD. Additional anti-TL1A drugs, afimkibart and duvakitug, are progressing rapidly through clinical development pipeline across multiple indications, underscoring the broad therapeutic potential of TL1A blockade. This review delineates the pathomechanistic basis of anti-TL1A therapies and explores emerging clinical applications. Moreover, to facilitate precision medicine approaches and optimize therapeutic outcomes among different population subgroups, we analyse the potential impact of genetic polymorphisms on individual responses to TL1A-targeted therapy. Taken together, anti-TL1A therapies hold considerable promise for modulating adaptive and immune pathways and represent an innovative strategy for treating complex inflammatory diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572242","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":"A Comprehensive Review of IL-10 and IL-10 Receptor Deficiencies: From Basic Science to Clinical Bedside.","authors":"Jun Xiao, Ziqing Ye, Ying Huang","doi":"10.1007/s12016-026-09154-6","DOIUrl":"10.1007/s12016-026-09154-6","url":null,"abstract":"<p><p>Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine. IL-10 receptor (IL-10R) consists of two chains of ligand-binding IL-10RA and two subunits of IL-10RB. IL-10 and IL-10R play important role in maintaining immune homeostasis in the gastrointestinal tract. Mutations in the IL10, IL10R cause spontaneous colitis in mice model and very early onset inflammatory bowel disease (VEOIBD) in human. Patients who have disease onset before 6 years of age are defined as VEOIBD. IL10 and IL10 receptor defect are classified as one type of monogenic inborn errors of immunity (IEI). IL-10 signalling defects demonstrate a Mendelian inheritance pattern with complete penetrance of intestinal inflammation. Patients develop symptoms during infancy and have more severe phenotype than polygenic inflammatory bowel disease (IBD). Here, we review the recent advances in the genetic mechanism, population dynamics and innate and adaptive immune dysregulation and interactions of gut microbiota regarding IL-10 signalling defects. The understanding of the pathogenesis has informed therapeutic strategies including haematopoietic stem cell transplant and novel biologics such as interleukin 1 receptor antagonist. Optimised transplant regimen and decreased risk of graft versus host disease with gut immunomodulation with vedolizumab might be used to improve transplant outcomes. More recently, gene therapy and gene editing have become treatment options for a range of IEIs, however evidence for IL-10 signalling defects is limited to in vitro and in vivo models. Beyond the Mendelian disorders, IL-10 signalling and neutralizing autoantibodies against IL-10 is relevant to the pathogenesis of polygenic IBD.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520302","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":"Unmasking the Impact of Air Pollution on Allergic Rhinitis.","authors":"Yingyang Xu, Xiaohong Lyu, Yongshi Yang, Nicole Akar-Ghibril, Marta Telatin, Rui Tang, Christopher Chang, Jinlyu Sun","doi":"10.1007/s12016-026-09155-5","DOIUrl":"10.1007/s12016-026-09155-5","url":null,"abstract":"<p><p>Allergic rhinitis (AR) is a chronic, non-infectious inflammatory condition of the nasal mucosa, primarily mediated by immunoglobulin E (IgE). Over the past decades, there has been a steady rise in the prevalence of AR worldwide, underscoring its growing public-health relevance. While genetic predisposition plays a role in AR development, environmental factors, particularly air pollution, have emerged as critical contributors. This review comprehensively examines epidemiological evidence linking air pollutants—such as particulate matter, hazardous gases, traffic-related air pollution (TRAP), volatile organic compounds (VOCs), and environmental tobacco smoke (ETS)—to AR prevalence and severity. Furthermore, it explores the synergistic interactions between air pollutants and inhaled allergens, highlighting mechanisms through which air pollution exacerbates AR. These mechanisms include disruption of nasal epithelial barrier function, enhancement of IgE-mediated hypersensitivity, oxidative stress, amplification of inflammatory responses, epigenetic modifications, alterations in microbial communities, and neurogenic regulation. Despite significant advances, the complex interplay between air pollutants and AR is not yet fully delineated. Emerging fields such as epigenetics and microbiomics offer promising directions for future research. This review aims to deepen understanding of the impact of air pollution on AR, providing insights and foundations for improved prevention and management strategies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510017","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":"Mouse Models of Food Allergies: Where Do They Take Us?","authors":"Shanshan Li, Zhanling Liang, Muhammad Mazhar, Yun Liao, Kin-Ming Kwan, Ping-Chang Yang, Ka-Hou Chu, Xiaoyu Liu, Xiaojun Xiao","doi":"10.1007/s12016-026-09146-6","DOIUrl":"10.1007/s12016-026-09146-6","url":null,"abstract":"<p><p>The rising prevalence of food allergies has coincided with the increasing use of animal models to study disease mechanisms and potential therapeutic strategies. Animal models, particularly murine models, have been instrumental in elucidating the mechanisms of allergic sensitization, effector responses, and potential therapeutic interventions. However, despite their utility, mouse models do not fully replicate human immune responses, limiting clinical translation. This review highlights conventional inbred mouse strains, genetically modified, and humanized mouse models, focusing on commonly used strains and key experimental variables, including allergen sources, adjuvants, and sensitization routes. Evaluation methods including anaphylaxis scoring, immunological profiling and histological analysis, ensure model reliability. Advances such as genetic modifications, humanized immune components, and multi-omics approaches aim to improve model relevance, facilitating better translation to clinical applications.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510051","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":"Evolving Therapeutic Strategies in ANCA-Associated Vasculitis: Current Standards and Emerging Targets for GPA and MPA.","authors":"Roberto Dal Pozzolo, Luca Iorio, Federica Davanzo, Elisabetta Zanatta, Luca Iaccarino, Roberta Ramonda, Roberto Gerli, Andrea Doria, Giacomo Cafaro, Roberto Padoan","doi":"10.1007/s12016-026-09147-5","DOIUrl":"10.1007/s12016-026-09147-5","url":null,"abstract":"<p><p>Granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) are severe autoimmune disorders characterized by necrotizing small-vessel inflammation, and are classified among anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV). Standard induction therapy combines glucocorticoids (GCs) with rituximab (RTX) or cyclophosphamide (CYC), with growing emphasis on GC minimization and selective use of avacopan in patients at high risk of GC toxicity. For maintenance therapy, fixed-interval RTX generally outperforms conventional oral agents and biomarker-guided re-dosing in unselected populations, yet treatment should be individualized. Persistent challenges include treatment-related toxicity, refractory manifestations, and defining safe discontinuation strategies. Expanding knowledge of AAV immunopathogenesis has driven the development of novel, mechanism-based therapies. These include agents targeting B cells and plasma cells (anti-CD38, anti-CD19, proteasome inhibition, CAR-T cells), complement components, and T-cell co-stimulation or cytokine networks (abatacept, IL-6 and JAK-inhibitors). Collectively, these advances are shifting AAV care from broad immunosuppression toward precision immunotherapy aimed at durable remission with reduced GC exposure and minimized long-term toxicity.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13006476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497757","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":"Conductive Mechanisms of Olfactory Dysfunction in Chronic Rhinosinusitis: A Focus on Nasal Airflow Dynamics and Olfactory Mucus.","authors":"Xincen Jiang, Lina Chen, Xingchen Pan, Yankun Li, Yinghong Zhang, Dawei Wu","doi":"10.1007/s12016-026-09149-3","DOIUrl":"10.1007/s12016-026-09149-3","url":null,"abstract":"<p><p>Olfactory dysfunction (OD) secondary to chronic rhinosinusitis (CRS) significantly impairs quality of life by hindering the detection of warning signals and reducing nutritional satisfaction. CRS, a prevalent inflammatory condition, commonly leads to diminished or complete loss of smell. A substantial component of CRS-associated OD is conductive, stemming from impaired odorant delivery to the olfactory neuroepithelium. The tools for assessing conductive OD range from clinical evaluations like endoscopy and CT scoring of the olfactory cleft to objective measures of nasal patency and advanced computational fluid dynamics modeling. The underlying conductive mechanisms are multifactorial, primarily involving two interrelated pathways: alterations in nasal airflow dynamics due to anatomical variations or obstructive lesions, and pathological changes in the physicochemical properties of olfactory cleft mucus. Obstructions from septal deviation, turbinate hypertrophy, nasal polyps, and mucosal edema within the olfactory cleft disrupt and redistribute inspiratory airflow, critically reducing odorant access. Concurrently, inflammation-driven changes in the olfactory mucus—including hypersecretion, ionic imbalance, and deficiencies in odorant-binding proteins and metabolizing enzymes—impair odorant transport, solubilization, and signal transduction. Current therapeutic strategies, such as endoscopic sinus surgery and corticosteroids, aim to relieve these conductive barriers but may offer only partial or temporary benefit, highlighting the need for precise phenotyping. A systematic, individualized assessment of both airflow patterns and mucus properties is crucial for understanding the conductive contribution and predicting outcomes. This review synthesizes current evidence on the conductive mechanisms of olfactory loss in CRS, evaluating the impact of nasal aerodynamics and mucus alterations, and discusses integrated management strategies for this debilitating condition.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13005826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493634","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":"Clinical Factors Associated with Genetically Confirmed Inborn Errors of Immunity in Children Presenting with Immune Dysregulation.","authors":"Oksana Boyarchuk, Anna Hilfanova, Valery Petrova, Tetiana Kovalchuk, Jolan E Walter","doi":"10.1007/s12016-026-09148-4","DOIUrl":"10.1007/s12016-026-09148-4","url":null,"abstract":"<p><p>BACKGROUND: Inborn errors of immunity (IEI) are increasingly recognized as important underlying causes of immune dysregulation in children. While recurrent infections remain a classical hallmark of IEI, non-infectious manifestations such as autoimmunity, lymphoproliferation, and autoinflammation are often the dominant or presenting features, posing diagnostic challenges. OBJECTIVE: To identify clinical features associated with IEI in children presenting with manifestations of immune dysregulation. METHODS: We conducted a multicenter retrospective–prospective cohort study including 106 children with manifestations of immune dysregulation evaluated at tertiary centers. Patients were stratified according to the presence or absence of genetically confirmed IEI. RESULTS: The group with genetically confirmed IEI comprised 67 patients, whereas the group with immune dysregulation without confirmed IEI comprised 39 patients. Several clinical features were significantly associated with genetic confirmation of IEI, including multilineage cytopenia (OR 6.27, 95% CI 1.74–22.59), Evans syndrome (OR 8.29, 95% CI 1.03–66.47), and lymphoproliferation (OR 4.20, 95% CI 1.55–11.35). Combined immune dysregulation phenotypes, such as autoimmunity with lymphoproliferation (OR 2.88, 95% CI 1.05–7.86) and autoimmunity with infections (OR 2.82, 95% CI 1.24–6.38), were also associated with genetic confirmation of IEI. Among genetically confirmed cases, disorders of immune dysregulation represented the largest subgroup (37.3%), followed by predominantly antibody deficiencies (31.3%) and syndromic or combined immunodeficiencies (16.4%). CONCLUSIONS: Specific patterns of immune dysregulation, particularly multilineage cytopenias, Evans syndrome, lymphoproliferation, and combined autoimmune phenotypes, were associated with genetically confirmed IEI in this cohort. Recognition of these clinical features may support earlier consideration of underlying IEI and help refine diagnostic decision-making in children presenting with immune dysregulation. </p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490783","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":"Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.","authors":"Felix I L Clanchy, Richard O Williams, Trevor W Stone","doi":"10.1007/s12016-025-09126-2","DOIUrl":"10.1007/s12016-025-09126-2","url":null,"abstract":"<p><p>The expression of the ionotropic glutamate receptors AMPAR and NMDAR has been measured on circulating leucocytes, particularly CD4+ lymphocytes, in many studies over the last two decades. As there are agonists and antagonists for these receptors that do not cross the blood brain barrier, they represent potential new avenues to target leucocytes in human disease. To determine the range of expression across pathological conditions, we compared the expression of AMPAR and NMDAR, as well as kainate receptors and metabotropic receptors, in 12 clinical studies including inflammatory autoimmune disease (rheumatoid arthritis, juvenile idiopathic arthritis, lupus and multiple sclerosis), breast cancer, viral infection, schizophrenia and in vitro studies. We measured the expression of AMPAR and NMDAR in freshly isolated CD4+ T cells, stimulated PBMC and myeloid cells (HL-60, THP-1 and monocyte-derived macrophages) using TaqMan qPCR. We found the gene expression of glutamate receptors to be negligible with few exceptions. We measured low but reproducible expression of GRIA3 in THP-1 pro-monocytic cells and human blood dendritic cell subsets (pDC, cDC1, cDC2). We observed that AMPA pre-treatment caused a greater inflammatory response in TNF-stimulated THP-1 cells. While these data illustrate a contradiction in the literature, the limited but reproducible expression of glutamate receptors in select immune subsets potentiates peripheral therapeutic targeting in specific disease contexts.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13002694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484408","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}