JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY变态反应与临床免疫学杂志
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY(英文缩写 J ALLERGY CLIN IMMUN),ISSN 0091-6749,eISSN 1097-6825,中文译名:变态反应与临床免疫学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 14.290 | Q1 |
| 2022 | 14.200 | Q1 |
| 2023 | 11.400 | Q1 |
| 2024 | 11.200 | Q1 |
| 2025 | 11.700 | Q1 |
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 最新收录文献
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1. Scientific Advances from Sharing URECA Data in Collaborative Analyses.
PMID:日期:2026-10-01The NIH-sponsored Urban Environment and Childhood Asthma (URECA) study of families in low-income, urban neighborhoods has provided important insights in this population but has a limited capacity to investigate risk factors across broader geographic and sociodemographic settings. To overcome this shortcoming, URECA investigators have shared data with multiple NIH-sponsored birth cohorts and investigators, including the Environmental Influences on Child Health Outcomes program and the Children's Allergy and Asthma Data Repository. We collaboratively developed methods, including a novel array to measure DNA methylation at CpG sites implicated in asthma, and geospatial estimates of exposure to air pollution, social conditions, and neighborhood characteristics based on residential address. Applying these tools to pooled datasets demonstrated associations between increased asthma incidence and birth in low-income, historically redlined census tracts, residence in low-food-access census tracts, identifying as African American or Caribbean-Hispanic American, and higher air pollution. Distinct asthma phenotypes based on longitudinal patterns of clinical features were associated with specific genetic polymorphisms. Studies of nasal cells identified patterns of gene expression and nasal epithelial DNAm signatures associated with specific asthma and allergy phenotypes. These collaborative projects have advanced our understanding of childhood asthma and established an investigative culture of data sharing, trust, and cooperation.
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2. SERPINE1 promoter variants and differential airway responses to virus and biological therapy.
2. SERPINE1启动子变异与病毒及生物治疗的气道差异反应PMID:日期:2026-10-01A common functional promoter polymorphism (4G4G/4G5G) in the SERPINE1 gene, which encodes the plasminogen activator inhibitor 1 (PAI-1) protein, is associated with more frequent asthma exacerbations. We examined genotype-specific airway transcriptomic responses during viral illness and how genotype modulates these responses in asthma exacerbations with and without mepolizumab treatment. Nasal lavage samples from a subset of children aged 6-17 years with exacerbation-prone asthma from the type 2-enriched urban asthma MUPPITS-1 and MUPPITS-2 cohorts were used for RNA sequencing and genetic studies. Expression quantitative trait locus (eQTL) analysis and weighted gene coexpression network analysis were performed to determine PAI-1 genotype modulation of gene expression during viral illness and genotype associations with mean expression levels of coexpressed networks of genes (modules). Linear regression analysis was performed to evaluate interactions between mepolizumab and the PAI-1 promoter variants. Risk genotypes were associated with lower SERPINE1 expression at baseline but higher levels over the course of viral illness (P < .02). In those with the risk allele at times of viral illness, there was increased expression of 4 coexpressed networks of genes including immune/Toll-like receptor signaling, and decreased expression of one network (ribosome). Subjects with the risk allele receiving mepolizumab with nonexacerbation viral illness had higher expression of eosinophil and mucus hypersecretion gene networks. In subjects with the risk allele receiving mepolizumab who experienced exacerbation, eosinophilic signaling networks were decreased, but gene networks involved in TGF-β/SMAD3 and perturbed epithelial integrity were increased compared to placebo. A number of drug-gene interactions were significant (P < .05, false discovery rate). Nasal lavage SERPINE1 transcripts increase during viral illness in children with asthma who have the risk allele but not in children without this allele. In asthma exacerbations, the risk allele is associated with augmentation of TGF-β/SMAD3 and epithelial pathways as well as a differential airway transcriptomic response to the type 2 modulator mepolizumab.
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3. Epidermal HLA-DQB1 exerts negative regulation of mast cell activation through the TSLP-driven SPP1-expressing macrophage axis.
PMID:日期:2026-09-26Keratinocytes(KCs) and the major histocompatibility complex class II (MHC-II) are implicated in inflammatory skin diseases. However, the precise expression profiles and causal role of keratinocyte -intrinsic MHC-II in urticaria remain largely undefined. To investigate the causal relationship and functional mechanism of epidermal MHC-II in IgE-mediated skin inflammation. Mendelian randomization (MR) and immunohistochemistry were employed to evaluate the genetic and clinical relevance of MHC-II in urticaria. A keratinocyte--specific H2-Ab1 knockout mouse model(K14H2-Ab1) was generated, and IgE induced passive cutaneous anaphylaxis(PCA) was assessed. Functional validation was performed using pharmacologic activation/inhibition. Immune responses and identify downstream signaling pathways were characterized using flow cytometry, single-cell RNA sequencing(scRNA-seq), chromatin immunoprecipitation (ChIP) assay, RNA interference, luciferase reporter gene assays, and western blotting. MR analysis identified a protective causal effect of skin HLA-DQB1 expression on urticaria risk. Epidermal MHC-II levels negatively correlated with disease severity and positively correlated with disease control scores in patients. Epidermal H2-Ab1 knockout exacerbated PCA responses in mice. Mechanistically, deletion of HLA-DQB1/H2-Ab1 in KCs reduced repressive H3K9me3 histone methylation at the TSLP promoter via downregulation of Suv39h1, leading to TSLP overexpression. TSLP promoted STAT5-dependent secreted phosphoprotein 1(SPP1) expression in macrophages, polarizing a pro-inflammatory SPP1 subset. SPP1 directly activated mast cells, enhancing degranulation and inflammatory mediator release. This KC-macrophage-MC axis was validated in co-culture systems. Epidermal HLA-DQB1/H2-Ab1 negatively regulates IgE-mediated skin inflammation by epigenetically suppressing TSLP expression, thereby restraining a TSLP-SPP1 macrophage-MC activation cascade. These findings reveal a novel immunoregulatory function of keratinocyte MHC-II and highlight the HLA-DQB1-TSLP-SPP1 macrophage axis as a potential therapeutic target in urticaria.
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4. Selective KIT-inhibition Supports Mast Cells as Key Drivers of Allergic Asthma Pathogenesis.
4. 选择性KIT抑制支持肥大细胞作为过敏性哮喘发病机制的关键驱动因素PMID:日期:2026-09-26Asthma is a chronic respiratory disease characterized by airway inflammation, airway hyperresponsiveness (AHR) and airway remodeling. Mast cell numbers are increased in asthmatic airways and contribute to bronchoconstriction and inflammation; yet their role in asthma development remains elusive. To investigate mast cell contributions to allergic asthma by pharmacologically targeting KIT, a central regulator of mast cell survival and activation, using the selective inhibitor THB001. THB001 effects were assessed in human lung mast cells (HLMCs), isolated human bronchi, and guinea pig trachea. To probe mast cell contributions in vivo, guinea pigs were subjected to a house dust mite (HDM)-induced asthma model and treated with THB001. HDM-induced bronchoconstriction was recorded after each challenge. At the endpoint, airway responsiveness was evaluated, followed by bronchoalveolar lavage fluid and lung tissue collection for histological, biochemical and transcriptomic analyses. THB001 suppressed KIT-dependent mast cell functions, inhibiting HLMCs degranulation and survival, and attenuating anti-IgE-induced bronchial contraction. In guinea pig tracheal segments, THB001 reduced HDM-induced responses, coinciding with a reduction in mast cells. In vivo, THB001 remodeled HDM-induced transcriptional signatures and lipid mediator release, prevented HDM-induced bronchoconstriction and AHR, and largely reversed HDM-induced increases in mast cells, inflammation, airway smooth muscle layer thickening and collagen deposition, with partial reduction of mucus-producing cells. Mast cell-dependent signaling is a key driver of allergic asthma pathogenesis. Pharmacological inhibition of KIT effectively suppresses mast cell activity and prevents hallmark functional and structural features of asthma in a guinea pig model, supporting KIT inhibition as a potential therapeutic approach for allergic asthma.
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6. Mechanistic and Clinical Updates in Chronic Rhinosinusitis: 2023-2025.
PMID:日期:2026-09-21Chronic rhinosinusitis (CRS) is a chronic inflammatory condition of the nose and paranasal sinuses associated with poor quality of life and high health care burden. CRS is broadly classified into two subtypes based on whether nasal polyps are present (CRSwNP) or absent (CRSsNP). While CRSsNP is more prevalent, the underlying mechanisms contributing to CRSwNP pathogenesis have been more extensively defined over the years. CRSwNP is characterized by type 2 (T2) inflammation as well as epithelial barrier dysfunction and in the past 3 years, a new endotype has been defined, inflammatory cell heterogeneity has been identified, novel cell populations have been discovered, and mechanisms contributing to epithelial barrier dysfunction have been advanced. Clinically, 4 biologics targeting T2 inflammation are now approved for CRSwNP. As these therapies become increasingly common in clinical practice, ongoing investigations have focused on comparing their efficacy and defining their role alongside more established interventions such as corticosteroids and sinus surgery. In this review, novel mechanistic findings and recent clinical developments in CRS between 2023 and 2025 will be highlighted.
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7. Standardised Human Phenotype Ontology Annotation Enables High Quality Phenotypic Data Capture in a Real-World Common Variable Immunodeficiency Cohort.
7. 标准化人类表型本体注释使真实世界常见变异型免疫缺陷队列中能够实现高质量表型数据采集PMID:日期:2026-09-21Patients with Common Variable Immunodeficiency (CVID) exhibit diverse clinical manifestations, indicating heterogeneity in pathogenic mechanisms. Systematic application of standardised phenotyping in large cohorts is essential to dissect this heterogeneity. The Human Phenotype Ontology (HPO) provides a structured framework for capturing and comparing disease phenotypes. To evaluate the application of systematic HPO-based phenotyping in CVID patients enrolled for whole-genome sequencing in a large national adult primary immunodeficiency cohort. We developed a web-based Phenotype Capture Tool and delivered structured clinician training to standardise HPO annotation. Numerical laboratory parameters were mapped to corresponding HPO terms to enrich patient records. We coded the phenotypes of 526 CVID patients across 11 UK centres. Clinician training increased phenotype granularity and improved phenotyping consistency between clinicians. We assigned 883 unique HPO terms across the cohort and applied logical rules to the terms to classify patients into an infection-only group and a complex phenotype group (42% vs 58%, respectively). Patients in the complex phenotype group were significantly more likely to have reduced switched memory and expanded CD21 B cells, as well as pathogenic variants in IUIS-listed genes overall and pathogenic NFKB1 variants specifically. Having a pathogenic variant in an IUIS-listed gene was associated with Autoimmune hemolytic anemia [HP:0001890] and having a pathogenic NFKB1 variant specifically was associated with Autoimmune neutropenia [HP:0001904]. This is the first study to systematically collect granular HPO-coded phenotypes in a large real-world CVID cohort, refining the CVID landscape and providing a comprehensive CVID HPO term set relevant for international research.
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8. Developments in Mast Cell Research.
8. 肥大细胞研究进展PMID:日期:2026-09-21This review summarizes major advances in mast cell (MC) research published between January 2024 and December 2025. Recent discoveries have reshaped our understanding of MC biology, revealing previously unrecognized roles in brain development, mucosal immunity, neuroimmune communication, and cancer. High-resolution structural studies have provided new insights into high affinity receptor for immunoglobulin (Ig)E (FcεRI) signaling, while emerging evidence has expanded the functional repertoire of inflammasome components and established Mas-related G-protein coupled receptor member (MRGPRX)2 as a central receptor mediating IgE-independent MC activation. Single-cell transcriptomic and spatial profiling studies have uncovered remarkable MC heterogeneity, identifying specialized populations with distinct homeostatic and pathogenic functions across tissues. These findings have also redefined the contribution of MCs to early-life allergic disease, anaphylaxis, pain, infection, and tumor immunity, highlighting their context-dependent functions. In parallel, major therapeutic advances-including antibodies targeting the KIT-stem cell factor (SCF) axis, next-generation anti-IgE therapies, Bruton's tyrosine kinase (BTK) inhibitors, and strategies targeting type 2 inflammatory pathways-are accelerating the development of more selective treatments for MC-driven disorders. Advances in experimental platforms, including human skin MC cultures, receptor-humanized and humanized mouse models, and computational pathology, are further expanding the tools available to investigate MC biology and accelerate translational research. Together, these conceptual, technological, and therapeutic advances are shaping the next generation of MC-targeted therapies.
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10. ABACHAI - Safety and efficacy of abatacept (s.c.) in patients with CTLA4 insufficiency or LRBA deficiency, a phase II clinical trial.
10. ABACHAI - 阿巴西普（皮下注射）在CTLA4缺陷或LRBA缺陷患者中的安全性和有效性，一项II期临床试验PMID:日期:2026-09-19Heterozygous germline mutations in CTLA4 (CTLA-4 insufficiency) and biallelic mutations in LRBA (LRBA deficiency) cause immune dysregulation with autoimmunity, lymphoproliferation, and immunodeficiency. For treatment, abatacept has been used successfully and is increasingly being used off-label; however, prospective clinical trial data are missing. To evaluate the safety and efficacy of abatacept in patients with CTLA-4 insufficiency or LRBA deficiency. ABACHAI was a prospective, open-label, single-arm phase IIa trial. Adult patients with genetically confirmed CTLA-4 insufficiency or LRBA deficiency and at least one clinically significant organ manifestation received 125 mg abatacept subcutaneously once weekly for 12 months. The primary endpoint was safety, defined as the number of episodes of failed infection control. Secondary endpoints included additional safety parameters, efficacy outcomes, and patient-reported quality of life. Twenty patients were enrolled (18 with CTLA-4 insufficiency and 2 with LRBA deficiency). Three patients had five severe infections during treatment (incidence rate 0.27 per patient-year), comparable to the year preceding enrolment. No EBV or CMV reactivations occurred. Abatacept reduced lymphoproliferation and immune activation and improved patient-reported quality of life and gastrointestinal symptom quality. Cytopenias and renal involvement were not sufficiently controlled. Four patients (20%) discontinued - three due to unrelated serious adverse events, one due to non-compliance. ABACHAI was the first prospective interventional trial, examining abatacept treatment in CTLA-4 insufficiency and LRBA deficiency. Abatacept demonstrated a favourable safety profile and organ-specific efficacy with strongest responses in lymphoproliferation and immune activation. Patients with refractory cytopenias or progressive organ involvement may require additional or alternative therapeutic strategies.