JOURNAL OF AUTOIMMUNITY自身免疫杂志
JOURNAL OF AUTOIMMUNITY(英文缩写 J AUTOIMMUN),ISSN 0896-8411,eISSN 1095-9157,中文译名:自身免疫杂志 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 | 14.511 | Q1 |
| 2022 | 12.800 | Q1 |
| 2023 | 7.900 | Q1 |
| 2024 | 7.000 | Q1 |
| 2025 | 6.800 | Q1 |
JOURNAL OF AUTOIMMUNITY 最新收录文献
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1. {"_":"IL-15 drives antigen-independent increase in granzyme KB CD8 T cells enriched in rheumatoid arthritis joints.","sup":["+","+"]}
PMID:日期:2026-10-03CD8 T cells co-expressing granzymes K and B (GzmK + B+) are enriched in the joint compared with peripheral blood and have been implicated in the pathogenesis of rheumatoid arthritis (RA). However, it remains unclear whether the enrichment of GzmK+B+ subsets is specific to RA. In addition, the mechanism underlying the generation of GzmK + B + CD8 T cells remains unknown. Characteristics of CD8 T cells in the synovium of patients with RA and osteoarthritis (OA) were examined by a flow cytometer. Public database of single cell RNA sequence (scRNA-seq) of RA and OA synovium was analyzed, and the results were verified by in vitro culture experiments. Flow cytometric analysis of viral antigen-specific CD8 T cells identified by MHC class I tetramer was performed. GzmK+B+ subset in CD8 T cells was more enriched in RA than OA joint, whereas no difference was observed in the frequency of GzmK + B- subset. In silico analysis of public database recapitulated these results and suggested the transition from GzmK + B- to GzmK+B+ subset which is mediated by IL-15- but not TCR-signaling. IL-15 induced an increase in GzmK + B + CD8 T cells from RA and OA joints in vitro. Viral antigen specific bystander CD8 T cells in RA joints are also enriched of GzmK+B+ subset. Our results suggest that increased IL-15 in RA joints promotes bystander activation of CD8 T cells, leading to the enrichment of GzmK + B + CD8 T cells, which are implicated in the pathogenesis of RA.
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2. Depletion of regulatory T cells breaks self-tolerance and induces epidermolysis bullosa acquisita in resistant C57BL/6J mice.
PMID:日期:2026-10-02Pemphigoid diseases (PDs) are antibody-mediated autoimmune blistering diseases caused by loss of tolerance to basement membrane proteins such as type VII collagen (COL7), triggering pathogenic T and B cell responses. The contribution of regulatory T cells (T) to disease resistance remains unclear. Using a COL7 immunization-induced PD mouse model, we show that transient T depletion breaks tolerance and induces skin blistering in otherwise PD-resistant H2 mice. Disease occurred predominantly in females and was associated with impaired T recovery, early skin inflammation, altered B-cell homeostasis, and antigen-specific CD154 T cells. These findings identify T as critical regulators of susceptibility to PD.
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3. Single-cell transcriptomics reveal tissue-specific neutrophil heterogeneity and functional reprogramming in autoimmunity.
PMID:日期:2026-09-22Neutrophils are increasingly recognized as key regulators of autoimmune responses; however, the mechanisms by which their heterogeneity is influenced across various tissues in autoimmunity remain insufficiently understood. Here, using experimental autoimmune encephalomyelitis (EAE), we show that splenic and bone marrow neutrophils acquire both CD4 T cell suppressive and Th17-promoting capacities. In contrast, lung neutrophils exhibit predominantly CD4 T cell suppressive activity. We further identify three distinct neutrophil subsets, comprising Ki67 N0, Acvrl1 N1, and CD300ld N2 neutrophils. Functionally, CD300ld neutrophils are characterized by a pro-inflammatory phenotype, whereas CD300ld neutrophils demonstrate immunosuppressive activity, indicating tissue-specific properties of these cells. Mechanistically, EAE induces splenic extramedullary granulopoiesis, resulting in the generation of heterogeneous neutrophil subsets, with a notable enrichment of N2 neutrophils in the lung. Within this organ, a unique microenvironment further reprograms CD300ld neutrophils toward a more immunosuppressive state through pathways associated with lipid metabolism. Notably, analogous subsets are also observed in animal models of rheumatoid arthritis and systemic lupus erythematosus, as well as in patients with multiple sclerosis. Collectively, our findings illustrate that splenic extramedullary granulopoiesis creates a heterogeneous neutrophil landscape, which is further shaped by tissue-specific microenvironments, driving the functional plasticity of neutrophils in EAE. This framework defines distinct neutrophil subsets as potential targets for immunomodulatory intervention in autoimmune diseases.
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4. Serum perfluorooctane sulfonate and perfluorooctanoic acid concentrations and longitudinal systemic lupus outcomes.
4. 血清全氟辛烷磺酸和全氟辛酸浓度与系统性红斑狼疮纵向结局的关系PMID:日期:2026-09-17Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are persistent per- and polyfluoroalkyl substances (PFAS) with immunomodulatory properties, but their role in systemic lupus erythematosus (SLE) outcomes remains unclear. We examined whether serum PFOS and PFOA concentrations were associated with subsequent increase in disease activity and damage accrual in SLE. We studied patients from the McGill University Health Centre Lupus Registry. A random sub-cohort of 100 patients with physician-confirmed SLE was selected. Blood samples for measurements of 69 PFAS congeners were collected between July 1997 and January 2023 within an overall follow-up period from July 1997 to September 2025. PFOS and PFOA were the only congeners detected in >50% of samples. Outcomes were time to a ≥4-point increase in the SLE Disease Activity Index 2000 (SLEDAI-2K) and time to first increase in the Systemic Lupus International Collaborating Clinics Damage Index (SLICC-DI). Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) per interquartile range increase in PFOS and PFOA concentrations. During follow-up, 53 participants experienced a ≥4-point increase in SLEDAI-2K and 45 experienced an increase in SLICC-DI. Higher PFOS (HR = 1.15, 95% CI 1.01-1.31) and PFOA concentrations (HR = 1.29, 95% CI: 1.09-1.52) were associated with a greater hazard of a ≥4-point increase in SLEDAI-2K. Increased risk of damage accrual was also associated with PFOS (HR = 1.20, 95% CI 1.03-1.39). Higher serum PFOS concentrations were associated with increases in both SLE disease activity and damage accrual, whereas higher PFOA concentrations were associated with increased SLE disease activity.
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5. Increased CCL22 production in early rheumatoid arthritis development with potential impact on mucosal autoimmunity, joint inflammation and T cell recruitment to LAMP3+ dendritic cells.
5. 早期类风湿关节炎发展中CCL22生成增加，对黏膜自身免疫、关节炎症以及T细胞向LAMP3+树突状细胞的募集具有潜在影响PMID:日期:2026-09-16Understanding alterations in immune homeostasis can help early diagnosis and prevention in rheumatoid arthritis (RA). As joint pain often precedes RA onset, we analysed pain-associated immune mediators in individuals at risk of RA (RISK-RA) and in early untreated RA. Serum CCL22 levels were elevated in both groups, prompting us to further study its sources and effects in RA. CCL22 expression was examined in RISK-RA and RA cohorts, healthy controls, BAL cells of healthy smokers and cigarette smoke-exposed mice. Spatial transcriptomics, single-cell RNA sequencing, and flow cytometry were used to assess CCL22 and CCR4 expression in joints. The CCR4 inhibitor C-021 was evaluated in collagen antibody-induced arthritis (CAIA). Increased CCL22 levels were detected in current smokers, in all tested cohorts, and in cigarette-smoke exposed mice. Smoking was associated with CCL22 gene hypomethylation in BAL cells. CCL22 was also expressed in arthritic joints, potentially induced by inflammatory mediators such as M-CSF and GM-CSF. ScRNA-seq and synovial fluid cell analyses identified LAMP3+CCR7+ dendritic cells (DCs) as the most prominent producers of CCL22. CCR4 was expressed by Tregs and subsets of activated, proliferating and effector CD4 T cells. Beyond T cells, CCL22 may affect innate mechanisms as CCR4 inhibition altered cytokine expression in macrophages and DCs and decreased CAIA severity. CCL22-mediated T cell recruitment may contribute to the mucosal breach of tolerance in smokers. In joints, CCL22 could promote inflammation and recruit activated and regulatory T cells to LAMP3+ DCs, a subset characterised by robust T cell modulatory potential.
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6. Intercalated cells contribute to the immune responses in renal autoimmune disease.
6. 插入细胞在肾脏自身免疫性疾病中参与免疫反应PMID:日期:2026-09-16Autoimmune diseases are a major cause of acute and chronic kidney injury, driven by complex mechanisms involving autoantibodies and cellular immune responses that result in tissue damage. Intercalated cells (ICs), specialized renal epithelial cells responsible for proton secretion, are strategically positioned at the epithelial-immune interface, making them ideal sensors of stress signals and potential regulators of immune responses. To investigate the molecular mechanisms by which ICs crosstalk with immune cells during autoimmune kidney injury, we depleted Foxp3 regulatory T-cells (Tregs) by injecting diphtheria toxin (DT) into male and female Foxp3-DTR mice. This triggered robust renal autoimmune inflammation, characterized by infiltration of neutrophils, macrophages, and T- and B-cells, along with the formation of ectopic lymphoid-like structures. We found elevated renal autoantibodies in urine and serum, with antibody deposition in glomeruli and tubules. We identified several renal antigens targeted by autoantibodies, suggesting a potential role for these antigens in kidney injury. Damage included glomerular hypertrophy, proximal tubular injury, an increased urine albumin/creatinine ratio, and decreased urine output. Disruption of immune tolerance led to upregulation of inflammasome-related genes and IL-33 in ICs, which act as key alarmin signals that promote Treg activation and expansion. Despite their initial depletion, Tregs rebounded at 2 and 8 weeks, particularly the subsets expressing the IL-33 receptor and activation markers. Our findings reveal a novel IC-Treg crosstalk, a potential immune-regulatory mechanism mediated by the IL-33 pathway that promotes renal immune tolerance. Understanding the mechanisms behind autoimmune renal tubular injury is essential for developing targeted therapies and identifying suitable biomarkers.
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7. Whole-blood transcriptomics identifies a distinct metabolic and inflammatory signature in lupus arthritis compared with rheumatoid arthritis.
7. 全血转录组学鉴别出狼疮性关节炎与类风湿性关节炎相比具有独特的代谢和炎症特征PMID:日期:2026-09-15Lupus arthritis (LA) is a major determinant of clinical outcomes and treat-to-target strategies in systemic lupus erythematosus (SLE), yet its molecular basis remains elusive. Whole-blood RNA sequencing from 170 SLE [67 with active arthritis but quiescent disease in other organs; 42 with only mucocutaneous activity (mcSLE); 61 clinically inactive (iSLE)], 19 active rheumatoid arthritis (RA), and 72 healthy donors. Pathway enrichment, unsupervised WGCNA, deconvolution, k-means clustering, and druggability analyses were applied. Compared to mcSLE, LA patients demonstrated upregulation of ribosome/metabolism, while inflammatory pathways were significantly upregulated in mcSLE. Comparison between LA and RA revealed 769 differentially expressed genes, indicating upregulation of ribosome/metabolism and oxidative phosphorylation (OXPHOS) pathways in LA. Activated NK cells were significantly increased in LA compared to RA and mcSLE. Within SLE patients, interferon pathways were less upregulated in LA. Unsupervised analysis showed LA to be strongly linked to upregulation of "OXPHOS/metabolism" module and downregulation of the "Interferon" module. In contrast, mcSLE and iSLE were associated with "Interferon" and "T-cell" modules, respectively. RA was strongly associated with the "Innate immunity" module. LA patients were categorized into three distinct molecular clusters dominated by OXPHOS/metabolism pathways ("metabolism" cluster; n = 14), inflammatory pathways ("inflammation" cluster; n = 29), and both metabolic and inflammatory pathways ("mixed" cluster; n = 24). Druggability analysis revealed differential anticipated benefit from different compounds for each LA-cluster. Metabolic -rather than inflammatory-pathways are dominant in LA and may account in part for suboptimal responses to existing therapies. LA encompasses molecular subtypes, characterized by distinct pathophysiologic aberrancies potentially reversible by unique compounds.
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8. Autoantibodies in systemic sclerosis display a proinflammatory Fc glycosylation signature independent of systemic inflammation.
8. 系统性硬化症中的自身抗体表现出促炎性Fc糖基化特征，且独立于全身性炎症PMID:日期:2026-09-12Reduced IgG Fc galactosylation, reflected by elevated agalactosylated (G0) glycoforms, is a hallmark of autoimmune diseases and correlates with systemic inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Whether similar glycosylation alterations occur in disease-specific autoantibodies in the absence of systemic inflammation remains unknown. IgG Fc glycosylation was analyzed in systemic sclerosis (SSc), a disease characterized by fibrosis, vasculopathy, and autoimmunity rather than overt systemic inflammation. Anti-centromere protein B antibody-positive (ACA) and anti-topoisomerase I antibody-positive (ATA) SSc patients were studied in a discovery (n = 69) and validation dataset (n = 58), with age- and sex-matched healthy donors (HDs; n = 30 per dataset) as controls (total n = 187). Total and antigen-specific IgG were affinity-purified and analyzed by liquid chromatography-mass spectrometry. Fc glycosylation traits were quantified, and associations with CRP and ESR assessed. Compared with HDs, total IgG1 in SSc exhibited reduced galactosylation (p ≤ 0.01) and sialylation, and increased bisection. These alterations were more pronounced in antigen-specific IgG1, with both anti-CENP-B and anti-TOP1 IgG1 displaying increased fucosylation and bisection; and reduced galactosylation and sialylation compared with total IgG1 (all p ≤ 0.002). Anti-CENP-B IgG1 showed higher bisection than anti-TOP1 IgG1 (p = 0.001), whereas antigen-specific IgG2/3 and IgG4 glycoforms were predominantly detected in ATA patients. Despite significantly elevated autoantigen-specific G0 glycoform frequencies compared with total IgG1 (p < 0.0001 to p = 0.013), no significant correlations with CRP or ESR were observed (r < 0.24 for all). Findings were confirmed in the validation dataset. Autoantigen-specific IgG1 in SSc exhibits a proinflammatory Fc glycosylation profile in the absence of systemic inflammation, suggesting disease-specific or localized mechanisms underlying Fc glycan remodeling.
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9. Disease-activity-linked complement-coagulation interactions and persistent platelet activation in treatment-naïve systemic lupus erythematosus.
9. 未经治疗的系统性红斑狼疮中与疾病活动相关的补体-凝血相互作用及持续性血小板活化PMID:日期:2026-09-09Thrombosis is a major cause of morbidity and mortality in systemic lupus erythematosus (SLE). Although multiple prothrombotic pathways have been identified, most have been studied individually or after treatment initiation. We aimed to characterize interactions between prothrombotic pathways in treatment-naïve SLE using an integrated longitudinal approach. In a prospective inception cohort, 20 treatment-naïve SLE patients were studied at diagnosis and after 6 months of treatment. Ten predefined prothrombotic molecular systems were assessed using laboratory assays, plasma proteomics and N-terminomics. Interactions were evaluated using correlation networks, principal component analysis (PCA), and protein-protein interactions. Mean age was 42.7 years, 70% were female. Median SLEDAI-2K decreased from 13.5 (baseline) to 2 (6-month follow-up). High disease activity was characterized by an interconnected prothrombotic system network, which declined in eight of ten systems at low disease activity. Platelet activation remained elevated despite reduced disease activity. PCA demonstrated a platelet-dominated interaction profile in antiphospholipid antibody-positive patients. Proteomics and N-terminomics revealed activation of complement and coagulation pathways during active disease, with enrichment of pathway-specific proteolytic cleavages that attenuated following clinical improvement. In this treatment-naïve SLE cohort, prothrombotic biology was characterized by dynamic, disease-activity-associated interactions across multiple molecular systems rather than isolated pathway activation. While inflammatory and complement-coagulation activation attenuated with clinical improvement, platelet activation persisted at low disease activity, indicating a component of prothrombotic biology that did not parallel changes in clinical disease activity. These findings provide a mechanistic framework for understanding thrombo-inflammatory pathway changes following treatment in early SLE.
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10. Gender differences in health-related quality of life in axial spondyloarthritis, psoriatic arthritis and systemic sclerosis: a scoping review.
10. 中轴型脊柱关节炎、银屑病关节炎和系统性硬化症中健康相关生活质量的性别差异：一项范围综述PMID:日期:2026-09-07Axial spondyloarthritis (AxSpA), psoriatic arthritis (PsA) and systemic sclerosis (SSc) substantially affect health-related quality of life (HRQoL). Gender-related factors may influence health behaviours, coping and access to care. Yet, studies often do not distinguish sex from gender or specify how these variables are measured, limiting insight into gender as a multidimensional construct. To map how gender is conceptualised and operationalised in HRQoL studies among patients with AxSpA, PsA and SSc, and to summarise HRQoL differences between binary sex/gender groups. We searched PubMed, Web of Science, EMBASE, CINAHL and PsycINFO. Eligible studies were quantitative, examined sex, gender or sex/gender as a primary variable in relation to HRQoL in AxSpA, PsA or SSc and were published in English or Dutch. Two reviewers screened records and extracted data. We included 30 studies, most published since 2021. All operationalised sex/gender as a binary variable, most often reported as male/female or men/women, without clearly distinguishing biological sex from gender identity. None measured broader gender dimensions. Reported HRQoL differences therefore reflected binary sex/gender comparisons, rather than multidimensional gender analyses. Female/women groups generally had lower HRQoL than male/men groups, particularly in PsA and AxSpA. Evidence for SSc was limited to one study. Current HRQoL research in AxSpA and PsA and limited evidence in SSc, reflects binary sex/gender comparisons rather than multidimensional gender analyses. Mechanisms remain unclear because biological, psychosocial and gender-related constructs were not directly measured. Future studies should distinguish sex and gender more clearly and incorporate gender-related measures where appropriate.