Autoimmunity reviews最新文献_第10页

The efficacy and safety of monoclonal anti-TNF antibodies in the treatment of vascular Behçet's syndrome: A systematic review and meta-analysis 单克隆抗tnf抗体治疗血管性behet综合征的疗效和安全性：一项系统综述和荟萃分析。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-30 DOI: 10.1016/j.autrev.2025.103862

Yeling Liu , Jingwen Wu , Yiyuan Ao , Lu Li , Xiaoou Wang , Menghao Zhang , Xin Yu , Luxi Sun , Jinjing Liu , Wenjie Zheng

Objectives

This study is the first meta-analysis to evaluate the efficacy and safety of monoclonal anti-TNF antibodies in patients with vascular Behçet's syndrome (VBS).

Methods

A comprehensive literature search was conducted on PubMed, Embase, Cochrane Library, Medline Complete, and Web of Science. Pooled estimates of clinical response including complete response (CR) and partial response (PR), were calculated at 3, 6, and 12 months. Subgroup analyses were performed based on the specific monoclonal anti-TNF antibodies used. Additionally, pooled proportions of imaging response before and after 6 months were assessed.

Results

Twelve studies involving 297 patients were included. The pooled proportions of clinical CR were 64.1 % (95 %CI 28.7–93.9 %), 89.1 % (95 %CI 72.4–98.6 %), and 94.5 % (95 %CI 82.5–99.8 %) at 3, 6, and 12 months, respectively. Imaging response was achieved in 92.9 % (95 %CI 77.2–100 %) of patients within 6 months and 92.5 % (95 %CI 74.8–99.9 %) after 6 months. During follow-up, 26 patients experienced a relapse while on monoclonal anti-TNF antibodies treatment. Of the 43 patients who discontinued therapy due to response, 28 % (n = 12) experienced a relapse. Adverse events (AEs) were reported in 10 studies involving 42 patients, with 31 patients experiencing severe AEs, including 5 deaths.

Conclusions

Monoclonal anti-TNF antibodies are an effective treatment for VBS, demonstrating significant clinical and radiological efficacy with a favorable safety profile. Prevention of relapses and control of disease progression remain critical objectives in VBS management. Further validation of their efficacy through randomized controlled trials (RCTs) stratified by arterial and venous involvement is warranted to strengthen the evidence base and optimize therapeutic strategies.

目的：本研究是首个评价单克隆抗tnf抗体治疗血管性behaperet综合征（VBS）的疗效和安全性的荟萃分析。方法：在PubMed、Embase、Cochrane Library、Medline Complete和Web of Science上进行综合文献检索。在3个月、6个月和12个 月时计算临床反应的综合估计，包括完全缓解（CR）和部分缓解（PR）。根据使用的特异性单克隆抗tnf抗体进行亚组分析。此外，评估6 个月前后影像学反应的总比例。结果：纳入12项研究，共297例患者。临床CR的总比例64.1 %(95 %可信区间28.7 - -93.9 %),89.1 %(95 %可信区间72.4 - -98.6 %),和94.5 %(95 %可信区间82.5 - -99.8 %)在3、6和12 个月分别。92.9 %（95 %CI 77.2-100 %）的患者在6 个月内达到影像学应答，92.5 %（95 %CI 74.8-99.9 %）的患者在6 个月后达到影像学应答。在随访期间，26例患者在接受单克隆抗tnf抗体治疗时复发。在43名因缓解而停止治疗的患者中，28% % （n = 12）复发。在涉及42例患者的10项研究中报告了不良事件（ae），其中31例患者出现严重ae，包括5例死亡。结论：单克隆抗tnf抗体是治疗VBS的有效方法，具有显著的临床和放射学疗效，且具有良好的安全性。预防复发和控制疾病进展仍然是VBS管理的关键目标。通过按动脉和静脉受累程度分层的随机对照试验（RCTs）进一步验证其疗效，有必要加强证据基础并优化治疗策略。

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引用次数: 0

Chimeric antigen receptor cell therapy: A revolutionary approach transforming cancer treatment to autoimmune disease therapy 嵌合抗原受体细胞疗法：将癌症治疗转化为自身免疫性疾病治疗的革命性方法

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-23 DOI: 10.1016/j.autrev.2025.103859

Ruifan Wen , Binbin Li , Feifeng Wu , Jueyi Mao , Tasnim Azad , Yang Wang , Junquan Zhu , Xin Zhou , Haotian Xie , Xinying Qiu , Marady Hun , Jidong Tian , Liang Zhang , Kimsor Hong , Chuan Wen

Currently, autoimmune disorders are predominantly managed with broad-spectrum immunosuppressive agents and monoclonal antibodies, which can alleviate disease symptoms but are rarely curative and are frequently associated with significant adverse effects. Autoreactive B cells play a key role in the pathogenesis of many autoimmune diseases; however, B-cell-depleting therapies such as rituximab have shown limited efficacy in certain autoimmune diseases, primarily due to the persistence of autoreactive B cells within lymphoid tissues and sites of inflammation. Consequently, there is an urgent need for more effective and targeted therapies for patients with severe and refractory autoimmune conditions. In this context, recent advancements in genetic engineering have facilitated the application of cell-based therapies, which have transitioned from oncology to treating autoimmune diseases. Therapies utilizing chimeric antigen receptor (CAR) engineered immune cells have emerged as a promising and potentially curative approach. Clinical trials targeting CD19-expressing B cells in B cell–driven autoimmune diseases, such as systemic lupus erythematosus (SLE), have yielded encouraging results, demonstrating durable remissions in otherwise treatment-resistant cases. In addition, novel strategies are being developed to broaden the therapeutic scope of CAR-based therapies in autoimmunity, including chimeric autoantibody receptor (CAAR)-T cells designed to eliminate autoantigen-specific B cells selectively and CAR-engineered regulatory T cells (CAR-Tregs) aimed at achieving antigen-specific immune modulation and restoration of self-tolerance. Despite these advances, several challenges persist, including short and long-term safety concerns, limited in vivo persistence, and the high costs associated with personalized cell manufacturing. Innovations in CAR design, such as logic-gated CARs, inducible suicide switches, and universal CAR constructs, are under active investigation to enhance safety, control, scalability, and clinical accessibility.

目前，自身免疫性疾病主要使用广谱免疫抑制剂和单克隆抗体进行治疗，这些药物可以缓解疾病症状，但很少能治愈，而且经常伴有严重的不良反应。自身反应性B细胞在许多自身免疫性疾病的发病机制中起关键作用；然而，B细胞消耗疗法如利妥昔单抗在某些自身免疫性疾病中显示出有限的疗效，主要是由于淋巴组织和炎症部位内自身反应性B细胞的持续存在。因此，迫切需要对严重和难治性自身免疫性疾病患者进行更有效和更有针对性的治疗。在这种情况下，基因工程的最新进展促进了细胞疗法的应用，这些疗法已经从肿瘤学过渡到治疗自身免疫性疾病。利用嵌合抗原受体（CAR）工程免疫细胞的治疗已经成为一种有希望和潜在的治疗方法。针对表达cd19的B细胞在B细胞驱动的自身免疫性疾病（如系统性红斑狼疮（SLE））中的临床试验已经取得了令人鼓舞的结果，在其他治疗耐药的病例中显示出持久的缓解。此外，正在开发新的策略来扩大基于car的自身免疫治疗的治疗范围，包括嵌合自身抗体受体(CAAR)-T细胞，旨在选择性地消除自身抗原特异性B细胞，car -工程调节性T细胞（CAR-Tregs）旨在实现抗原特异性免疫调节和恢复自身耐受性。尽管取得了这些进展，但仍存在一些挑战，包括短期和长期的安全性问题、有限的体内持久性以及与个性化细胞制造相关的高成本。CAR设计方面的创新，如逻辑门控CAR、诱导式自杀开关和通用CAR结构，正在积极研究中，以提高安全性、可控性、可扩展性和临床可及性。

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引用次数: 0

Infectious agents in dilated cardiomyopathy: Genetic interactions, autoimmunity, mechanisms, and therapeutic approaches 扩张型心肌病的传染因子：遗传相互作用、自身免疫、机制和治疗方法

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-23 DOI: 10.1016/j.autrev.2025.103860

Jingdi Zhang, Haoting Zhan, Honglin Xu, Rongrong Wang, Zhan Li, Futai Feng, Hongzheng Wu, Zhixin Xu, Siyu Wang, Ye Guo, Yongzhe Li

Dilated cardiomyopathy (DCM) is a heterogeneous myocardial disorder characterized by left ventricular dilation and systolic dysfunction in the absence of ischemic, hypertensive, or valvular heart disease. Although its precise etiology remains unclear, it is widely recognized as a multifactorial disease arising from complex interactions between genetic predisposition and environmental triggers. Among these, infectious agents have been implicated in the pathogenesis of various subtypes, particularly inflammatory and idiopathic DCM. These agents can contribute to disease onset and progression through direct cardiomyocyte injury, immune-mediated chronic inflammation, and other yet-to-be-defined mechanisms. Infection-driven autoimmune activation is another potential key contributor to DCM, potentially linking infectious exposure to sustained myocardial damage. However, the precise role of various infectious agents in DCM initiation and progression, as well as their interactions with genetic predisposition and autoimmune activation, is inadequately understood. Improving understanding of infection-related etiologies could facilitate development of targeted therapeutic strategies; however, significant challenges persist in identifying causative and novel pathogens, and translating this into clinical practice. Therefore, this review explores the complex interactions between infectious agents, genetic predisposition, and autoimmune responses in DCM pathogenesis. We summarize current evidence on the role of infectious agents in DCM and emerging therapeutic strategies aimed at treating infection-related DCM. Finally, we outline future research directions to advance understanding of infection-associated DCM and improve patient outcomes. We reveal that a deeper understanding of host-microbe interactions, immune pathways, and genetic predisposition is essential for advancing DCM research. Furthermore, integrating genomics, metagenomics, and antibody and immunological profiling is crucial for developing personalized therapeutic strategies for this complex disease.

扩张型心肌病（DCM）是一种在没有缺血性、高血压或瓣膜性心脏病的情况下，以左心室扩张和收缩功能障碍为特征的异质心肌疾病。虽然其确切的病因尚不清楚，但它被广泛认为是一种多因素疾病，由遗传易感性和环境诱因之间的复杂相互作用引起。其中，感染因子涉及各种亚型的发病机制，特别是炎症性和特发性DCM。这些药物可以通过直接心肌细胞损伤、免疫介导的慢性炎症和其他尚未确定的机制促进疾病的发生和进展。感染驱动的自身免疫激活是DCM的另一个潜在关键因素，可能将感染暴露与持续的心肌损伤联系起来。然而，各种感染因子在DCM发生和进展中的确切作用，以及它们与遗传易感性和自身免疫激活的相互作用，尚不充分了解。提高对感染相关病因的了解有助于制定有针对性的治疗策略；然而，在识别致病病原体和新型病原体并将其转化为临床实践方面仍然存在重大挑战。因此，本文将探讨感染因子、遗传易感性和自身免疫反应在DCM发病机制中的复杂相互作用。我们总结了感染因子在DCM中的作用和针对治疗感染相关DCM的新治疗策略的现有证据。最后，我们概述了未来的研究方向，以促进对感染相关DCM的理解并改善患者的预后。我们揭示了对宿主-微生物相互作用，免疫途径和遗传易感性的更深入了解对于推进DCM研究至关重要。此外，整合基因组学、宏基因组学、抗体和免疫学谱对于开发针对这种复杂疾病的个性化治疗策略至关重要。

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引用次数: 0

Mesenchymal stem cell in immunomodulation of dendritic cells: Implications for inflammatory bowel disease therapy 树突状细胞免疫调节中的间充质干细胞：炎症性肠病治疗的意义。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-23 DOI: 10.1016/j.autrev.2025.103861

Dongqin Song , Chang'e He , Dickson Kofi Wiredu Ocansey , Bo Wang , Yunbing Wu , Fei Mao

Inflammatory bowel disease (IBD) is a highly prevalent and recurrent autoimmune disorder characterized by dysregulation of the immune system leading to intestinal inflammation. Currently, available clinical treatments, such as mesalazine, are mainly used to alleviate symptoms but do not cure the disease. Mesenchymal stem cells (MSCs), as an emerging therapeutic tool, show potential in IBD through immunomodulatory effects, but their specific mechanisms need further exploration. Dendritic cells (DCs) are important antigen-presenting cells that play a key role in the immune response in IBD, although their specific mechanism of action remains largely uncovered. This review focuses on discussing MSCs and their derived exosomes in the modulation of DC in IBD, providing insight into the therapeutic potentials of MSCs in IBD.

炎症性肠病（IBD）是一种高度流行和反复发作的自身免疫性疾病，其特征是免疫系统失调导致肠道炎症。目前，可用的临床治疗方法，如美沙拉嗪，主要用于缓解症状，但不能治愈疾病。间充质干细胞（Mesenchymal stem cells, MSCs）作为一种新兴的治疗工具，通过免疫调节作用在IBD中显示出潜力，但其具体机制有待进一步探索。树突状细胞（dc）是重要的抗原呈递细胞，在IBD的免疫应答中发挥关键作用，尽管其具体的作用机制仍未完全阐明。本文重点讨论了MSCs及其衍生外泌体在IBD中DC的调节，为MSCs在IBD中的治疗潜力提供了见解。

引用次数: 0

Impact and management of warm autoimmune haemolytic anaemia associated with systemic lupus erythematosus 与系统性红斑狼疮相关的温热自身免疫性溶血性贫血的影响和管理。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-23 DOI: 10.1016/j.autrev.2025.103858

Guillermo J. Pons-Estel , Marta Mosca , Daniel J. Wallace , Federico Zazzetti , Ann Leon , Wim Noël , Andreia Pierce , Tarek Ebrahim , Irina Murakhovskaya

Warm autoimmune haemolytic anaemia (wAIHA) is a rare autoantibody-mediated disorder that may occur in association with systemic lupus erythematosus (SLE). The clinical course of wAIHA is highly variable, ranging from anaemia compensated adequately by reticulocytosis to severe, life-threatening cases. While insights into the pathogenesis of wAIHA in SLE remain limited, emerging evidence highlights the risk factors and impact of wAIHA in the context of SLE. Management of wAIHA associated with SLE remains challenging as there is limited clinical evidence to support treatment decisions. New therapies, some that target underlying disease mechanisms relevant to both conditions, are in development. In this review, we examine the impact of wAIHA on clinical outcomes for patients with SLE, summarise the current management strategies along with unmet needs, and provide an update on novel therapeutic strategies.

温热自身免疫性溶血性贫血（wAIHA）是一种罕见的自身抗体介导的疾病，可能与系统性红斑狼疮（SLE）相关。wAIHA的临床病程变化很大，从网状细胞缺乏症充分补偿的贫血到严重的危及生命的病例。虽然对wAIHA在SLE中的发病机制的了解仍然有限，但新出现的证据强调了wAIHA在SLE背景下的危险因素和影响。由于支持治疗决策的临床证据有限，与SLE相关的wAIHA的管理仍然具有挑战性。一些针对与这两种疾病相关的潜在疾病机制的新疗法正在开发中。在这篇综述中，我们研究了wAIHA对SLE患者临床结果的影响，总结了当前的管理策略以及未满足的需求，并提供了新的治疗策略。

引用次数: 0

Radio-labelled fibroblast activation protein inhibitors in interstitial lung diseases – a systematic review 放射性标记成纤维细胞活化蛋白抑制剂在间质性肺疾病中的应用综述

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-20 DOI: 10.1016/j.autrev.2025.103856

Mads Bundgaard-Nielsen , Rikke Helin Johnsen , Jann Mortensen , Saher Burhan Shaker , Christoffer Tandrup Holst Nielsen

Background

Currently, no tools can monitor ongoing fibrotic activity properly, making early identification of and timely therapeutic intervention with antifibrotics in patients with progressive fibrosing interstitial lung disease (ILD) difficult. Fibroblast activation protein-α inhibitor (FAPI) radiotracers could address these challenges.

Objective

This review examines the association between pulmonary FAPI tracer uptake, fibrotic activity, and clinical parameters used for disease monitoring and prognostication in ILD to provide insights into its clinical potential.

Methods

In January 2025, a systematic literature search on PubMed, Ovid Medline, and Cochrane Library, utilizing the block-search strategy and snowballing, was conducted, and 13 studies were included.

Results

Both murine and human studies support that FAPI tracer uptake reflects fibrotic activity in ILDs, as uptake was consistently elevated in subject groups compared to controls. In murine ILD models, increased uptake was associated with fibrosis and fibroblast activation protein-α (FAP-α) expression upon histological examination. Uptake preceded the development of fibrosis on computed tomography (CT) and attenuated once fibrosis was established. In human ILD patients (Idiopathic pulmonary fibrosis (IPF) = 55, Connective tissue disease (CTD) ILD = 68, other ILDs = 55), FAPI uptake was localized to fibrotic lesions on high-resolution computed tomography (HRCT) and associated with increased FAP-α expression ex vivo. Uptake correlated with baseline pulmonary function tests (PFTs) and fibrosis extent on HRCT. Increased FAPI tracer uptake at baseline predicted disease progression upon follow-up.

Conclusion

An increasing body of evidence supports that FAPI tracers hold great clinical potential for the management of ILD by accurately monitoring fibrotic disease activity and identifying patients at risk of progression. Further research is required to confirm these findings.

背景：目前，没有工具可以适当地监测正在进行的纤维化活动，这使得进展性纤维化间质性肺疾病（ILD）患者的早期识别和及时的抗纤维化药物治疗干预变得困难。成纤维细胞活化蛋白-α抑制剂（FAPI）放射性示踪剂可以解决这些挑战。目的：本综述探讨肺FAPI示踪剂摄取、纤维化活性和用于ILD疾病监测和预后的临床参数之间的关系，以深入了解其临床潜力。方法：于2025年1月对PubMed、Ovid Medline和Cochrane Library进行系统文献检索，采用分组检索策略和滚雪球法，纳入13项研究。结果：小鼠和人类的研究都支持FAPI示踪剂的摄取反映了ild的纤维化活性，因为与对照组相比，受试者组的摄取持续升高。在小鼠ILD模型中，组织学检查显示，摄取增加与纤维化和成纤维细胞活化蛋白-α (FAP-α)表达有关。在计算机断层扫描（CT）上，摄取先于纤维化的发展，并在纤维化建立后减弱。在人类ILD患者（特发性肺纤维化（IPF） = 55，结缔组织病（CTD） ILD = 68，其他ILD = 55）中，高分辨率计算机断层扫描（HRCT）显示，FAPI摄取局限于纤维化病变，并与体外FAP-α表达增加相关。摄取与基线肺功能测试（PFTs）和HRCT纤维化程度相关。基线时FAPI示踪剂摄取增加预测随访时疾病进展。结论：越来越多的证据支持FAPI示踪剂通过准确监测纤维化疾病活动和识别有进展风险的患者，在ILD的管理中具有巨大的临床潜力。需要进一步的研究来证实这些发现。

{"title":"Radio-labelled fibroblast activation protein inhibitors in interstitial lung diseases – a systematic review","authors":"Mads Bundgaard-Nielsen , Rikke Helin Johnsen , Jann Mortensen , Saher Burhan Shaker , Christoffer Tandrup Holst Nielsen","doi":"10.1016/j.autrev.2025.103856","DOIUrl":"10.1016/j.autrev.2025.103856","url":null,"abstract":"<div><h3>Background</h3><div>Currently, no tools can monitor ongoing fibrotic activity properly, making early identification of and timely therapeutic intervention with antifibrotics in patients with progressive fibrosing interstitial lung disease (ILD) difficult. Fibroblast activation protein-α inhibitor (FAPI) radiotracers could address these challenges.</div></div><div><h3>Objective</h3><div>This review examines the association between pulmonary FAPI tracer uptake, fibrotic activity, and clinical parameters used for disease monitoring and prognostication in ILD to provide insights into its clinical potential.</div></div><div><h3>Methods</h3><div>In January 2025, a systematic literature search on PubMed, Ovid Medline, and Cochrane Library, utilizing the block-search strategy and snowballing, was conducted, and 13 studies were included.</div></div><div><h3>Results</h3><div>Both murine and human studies support that FAPI tracer uptake reflects fibrotic activity in ILDs, as uptake was consistently elevated in subject groups compared to controls. In murine ILD models, increased uptake was associated with fibrosis and fibroblast activation protein-α (FAP-α) expression upon histological examination. Uptake preceded the development of fibrosis on computed tomography (CT) and attenuated once fibrosis was established. In human ILD patients (Idiopathic pulmonary fibrosis (IPF) = 55, Connective tissue disease (CTD) ILD = 68, other ILDs = 55), FAPI uptake was localized to fibrotic lesions on high-resolution computed tomography (HRCT) and associated with increased FAP-α expression ex vivo. Uptake correlated with baseline pulmonary function tests (PFTs) and fibrosis extent on HRCT. Increased FAPI tracer uptake at baseline predicted disease progression upon follow-up.</div></div><div><h3>Conclusion</h3><div>An increasing body of evidence supports that FAPI tracers hold great clinical potential for the management of ILD by accurately monitoring fibrotic disease activity and identifying patients at risk of progression. Further research is required to confirm these findings.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 9","pages":"Article 103856"},"PeriodicalIF":9.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367847","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}

引用次数: 0

Advancing research on regulatory autoantibodies targeting GPCRs: Insights from the 5th international symposium 推进靶向gpcr的调节性自身抗体的研究：来自第五届国际研讨会的见解。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-19 DOI: 10.1016/j.autrev.2025.103855

Otavio Cabral-Marques , Lena F. Schimke , Guido Moll , Igor Salerno Filgueiras , Adriel Leal Nóbile , Anny Silva Adri , Fernando Yuri Nery do Vale , Júlia Nakanishi Usuda , Yohan Lucas Gonçalves Corrêa , Débora Albuquerque , Roseane Galdioli Nava , Ronaldy Santana Santos , Haroldo Dutra Dias , Hélio Fernandes Silva , Pedro Batista Marconi , Rusan Catar , Michael Adu-Gyamfi , Pinchao Wang , Taj Ali Khan , Alexander M. Hackel , Gabriela Riemekasten

The 5th International Symposium on Regulatory Autoantibodies Targeting GPCR (RAB-GPCRs) advanced the understanding of the significant role played by autoantibodies targeting G-protein-coupled receptors (GPCRs) in various human diseases. Once considered passive markers, RAB-GPCRs are now recognized as active modulators of cellular signaling, immune regulation, and inflammation. The symposium highlighted their involvement in multiple prominent pathologies, including autoimmune diseases, cardio- and cerebrovascular diseases, and neuroimmunologic disorders such as myalgic encephalomyelitis/chronic fatigue syndrome and post-COVID-19 syndrome (ME/CFS/PCS), as well as solid organ and hematopoietic stem cell transplantation (SOT/HSCT). Experts from rheumatology, immunology, and neurology presented interdisciplinary discussions on the potential of RAB-GPCRs as biomarkers and therapeutic targets. Advances in screening methods, biomarker identification, and therapeutic strategies were shared, emphasizing their diagnostic potential and application in novel therapeutic interventions. This report summarizes key insights from the symposium, particularly focusing on the modulatory properties of RAB-GPCRs and their relevance in both immune-mediated diseases and other pathologies (e.g., vascular, degenerative) that are traditionally not considered primarily immune-mediated. Ongoing research is expected to further establish these autoantibodies as crucial components in disease modulation and systems biology contexts, offering new opportunities for precision medicine and improved clinical outcomes in immune-related disorders.

第五届靶向GPCR的调节自身抗体国际研讨会（rabb -GPCR）促进了对靶向g蛋白偶联受体（GPCR）的自身抗体在各种人类疾病中的重要作用的认识。曾经被认为是被动标记物的rab - gpcr现在被认为是细胞信号、免疫调节和炎症的主动调节剂。研讨会强调了他们在多种重要病理方面的参与，包括自身免疫性疾病、心脑血管疾病、神经免疫疾病，如肌痛性脑脊髓炎/慢性疲劳综合征和covid -19后综合征（ME/CFS/PCS），以及实体器官和造血干细胞移植（SOT/HSCT）。来自风湿病学、免疫学和神经学的专家就rabb - gpcr作为生物标志物和治疗靶点的潜力进行了跨学科的讨论。在筛选方法、生物标志物鉴定和治疗策略方面的进展进行了分享，强调了它们的诊断潜力和在新型治疗干预中的应用。本报告总结了研讨会的主要见解，特别关注rab - gpcr的调节特性及其在免疫介导疾病和传统上不被认为主要是免疫介导的其他病理（例如血管、退行性疾病）中的相关性。正在进行的研究有望进一步确立这些自身抗体作为疾病调节和系统生物学背景下的关键组成部分，为精准医学和改善免疫相关疾病的临床结果提供新的机会。

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引用次数: 0

Systematic evaluation of the associations between schizophrenia and autoimmune diseases: An umbrella review 精神分裂症与自身免疫性疾病相关性的系统评价：概括性综述

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-16 DOI: 10.1016/j.autrev.2025.103854

Zhouyang Sun, Beibei Han, Qianlu Ding, Yuan Feng, Tingyi Jia, Yixin Ouyang, Xinru Guo, Jingyi Liang, Qianlong Huang, Changgui Kou , Wei Bai

Objective

This study aims to assess research trends in the association between schizophrenia and autoimmune diseases, systematically review their relationship, and evaluate the credibility of existing evidence.

Methods

Bibliometric analysis was conducted using the bibliometrix package in R, along with VOSviewer and CiteSpace. Relevant systematic reviews and meta-analyses were retrieved from six databases: PubMed, Web of Science, Embase, CINAHL, PsycINFO, and the Cochrane Library. Summary risk estimates were recalculated using the DerSimonian and Laird method under a random-effects model, and the credibility of the evidence was assessed.

Results

The bibliometric analysis found that “meta-analysis” has become a frequently used keyword and may be a focal point for future research. The umbrella review included 17 articles, containing 24 report data points from 12 quantitative reviews. Results indicated that 9 reports assessed the relationship between schizophrenia and autoimmune diseases. Schizophrenia was significantly associated with autoimmune neurological disorders (RR = 1.42; 95 % CI = 1.18–1.72), providing suggestive evidence. Seven reports evaluated the impact of schizophrenia on autoimmune diseases, showing highly suggestive evidence that schizophrenia patients had a pooled relative risk of 2.22 (95 % CI = 1.95–2.52) for psoriasis. Eight reports assessed the impact of autoimmune diseases on schizophrenia, with bullous pemphigoid patients showing significantly higher schizophrenia prevalence (OR = 2.63; 95 % CI = 2.03–3.39).

Conclusions

This study synthesizes evidence of varying levels, highlighting the association between schizophrenia and autoimmune diseases. It offers new insights for future exploration, fosters interdisciplinary collaboration, and provides valuable implications for public health policy development.

目的本研究旨在评估精神分裂症与自身免疫性疾病相关性的研究趋势，系统回顾两者之间的关系，并评估现有证据的可信度。方法使用R中的bibliometrix软件包，以及VOSviewer和CiteSpace进行文献计量学分析。相关的系统综述和荟萃分析从六个数据库检索：PubMed、Web of Science、Embase、CINAHL、PsycINFO和Cochrane图书馆。在随机效应模型下，使用DerSimonian和Laird方法重新计算总结风险估计，并评估证据的可信度。结果文献计量分析发现，“元分析”已成为一个频繁使用的关键词，并可能成为未来研究的重点。总括性审查包括17篇文章，包含来自12个定量审查的24个报告数据点。结果显示，9份报告评估了精神分裂症与自身免疫性疾病的关系。精神分裂症与自身免疫性神经系统疾病显著相关(RR = 1.42；95% CI = 1.18-1.72)，提供了启发性证据。七份报告评估了精神分裂症对自身免疫性疾病的影响，显示出高度暗含性的证据，精神分裂症患者患牛皮癣的总相对风险为2.22 （95% CI = 1.95-2.52）。8份报告评估了自身免疫性疾病对精神分裂症的影响，大疱性类天疱疮患者的精神分裂症患病率明显更高(OR = 2.63；95% ci = 2.03-3.39)。本研究综合了不同水平的证据，强调了精神分裂症与自身免疫性疾病之间的关联。它为未来的探索提供了新的见解，促进了跨学科合作，并为公共卫生政策的制定提供了宝贵的启示。

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引用次数: 0

Clinical features, pathogenesis, and treatment of inflammatory bowel disease-associated spondyloarthritis 炎症性肠病相关脊柱关节炎的临床特征、发病机制和治疗

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-15 DOI: 10.1016/j.autrev.2025.103853

Mitsuhiro Akiyama, Waleed Alshehri, Koji Suzuki, Kanako Shimanuki, Koichi Saito, Yuko Kaneko

Inflammatory bowel disease-associated spondyloarthritis (IBD-SpA) is a unique subtype of SpA that affects approximately 10–20 % of patients with IBD. It encompasses both peripheral arthritis and axial involvement, with enthesitis being increasingly recognized. Despite its clinical significance, there are currently no established screening tools, classification criteria, or standardized treatment guidelines specific to IBD-SpA. Management is typically guided by recommendations for IBD and SpA, requiring close collaboration between gastroenterologists and rheumatologists. Emerging evidence suggests that subclinical gut inflammation and IL-23–IL-17–TNFα signaling pathway play central roles in the pathogenesis of IBD-SpA. Among the available therapeutic options, TNF inhibitors and JAK inhibitors have demonstrated efficacy in both IBD and SpA, whereas IL-17 inhibitors may exacerbate intestinal inflammation. Additionally, vedolizumab, an α4β7 integrin inhibitor, while effective for IBD, has been implicated in triggering de novo SpA. These complexities highlight the need for a tailored treatment approach that balances efficacy for both gut and joint inflammation. This review provides an updated overview of the clinical features, diagnosis, pathogenesis, and treatment strategies for IBD-SpA, emphasizing recent advancements and future directions in the field.

炎症性肠病相关脊柱关节炎（IBD-SpA）是一种独特的SpA亚型，影响约10 - 20%的IBD患者。它包括外周关节炎和轴向受累，越来越多的人认识到关节炎。尽管具有临床意义，但目前尚无针对IBD-SpA的既定筛查工具、分类标准或标准化治疗指南。管理通常以IBD和SpA的建议为指导，需要胃肠病学家和风湿病学家之间的密切合作。新的证据表明，亚临床肠道炎症和IL-23-IL-17-TNFα信号通路在IBD-SpA的发病机制中起核心作用。在现有的治疗方案中，TNF抑制剂和JAK抑制剂已被证明对IBD和SpA都有效，而IL-17抑制剂可能会加剧肠道炎症。此外，vedolizumab，一种α4β7整合素抑制剂，虽然对IBD有效，但与触发从头SpA有关。这些复杂性突出了需要一种量身定制的治疗方法，以平衡肠道和关节炎症的疗效。本文综述了IBD-SpA的临床特征、诊断、发病机制和治疗策略，并强调了该领域的最新进展和未来发展方向。

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引用次数: 0

Autoreactive B cells in autoimmune diseases: Mechanisms, functions and clinical implications 自身免疫性疾病中的自身反应性B细胞：机制、功能和临床意义

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-08 DOI: 10.1016/j.autrev.2025.103851

Aurore Collet , Thomas Guerrier , Sébastien Sanges , Aurélien Chépy , Vincent Sobanski , David Launay , Sylvain Dubucquoi

Autoreactive B cells play a key role in the pathophysiology of autoimmune diseases (AIDs). Still, due to their low frequency in the circulating blood, they are less well characterized than the global B cell pool. This review aims at describing the tools that allow the study of autoreactive B cells, deciphering their features and functions, and discussing the therapeutic implications that arise from these findings.

The capacity to detect and analyze autoreactive B cells has been significantly improved by diverse techniques such as ELISpot and flow cytometry, shedding light on their roles in immune dysregulation. It reveals the multifaceted features of autoreactive B cells in terms of phenotypic and functional characteristics, that vary between different AIDs, and from one autoantigen to another. This heterogeneity may be influenced by factors such as the nature of the targeted autoantigen, or the costimulatory signals involved. These observations highlight that autoreactive B cells contribute not only to autoantibody production, but also to the perpetuation of autoimmunity through additional mechanisms, including antigen presentation and cytokine secretion. Recent therapeutic approaches have been developed to target autoreactive B cells, allowing an antigen-specific depletion of B cells, without causing widespread immunosuppression. Challenges remain, such as understanding the precise mechanisms by which the B cell tolerance breakdown occur, and the pathways by which autoreactive B cells activate (i.e. germinal centre or extrafollicular pathway). Ongoing research into the mechanisms regulating autoreactive B cells will be crucial for designing more targeted and effective therapies, leading to better outcomes for AID patients.

自身反应性B细胞在自身免疫性疾病（艾滋病）的病理生理中起着关键作用。尽管如此，由于它们在循环血液中的频率较低，它们的特征不如全球B细胞池。本综述旨在描述研究自身反应性B细胞的工具，解读其特征和功能，并讨论这些发现产生的治疗意义。通过ELISpot和流式细胞术等多种技术，检测和分析自身反应性B细胞的能力得到了显著提高，揭示了它们在免疫失调中的作用。它揭示了自身反应性B细胞在表型和功能特征方面的多方面特征，这些特征在不同的艾滋病之间以及从一种自身抗原到另一种自身抗原之间有所不同。这种异质性可能受到诸如靶向自身抗原的性质或所涉及的共刺激信号等因素的影响。这些观察结果强调，自身反应性B细胞不仅有助于自身抗体的产生，而且还通过其他机制，包括抗原呈递和细胞因子的分泌，促进自身免疫的延续。最近的治疗方法已经发展到针对自身反应性B细胞，允许抗原特异性B细胞的消耗，而不会引起广泛的免疫抑制。挑战仍然存在，例如了解B细胞耐受性破坏发生的确切机制，以及自身反应性B细胞激活的途径（即生发中心或滤泡外途径）。对自身反应性B细胞调节机制的持续研究将对设计更有针对性和更有效的治疗方法至关重要，从而为艾滋病患者带来更好的结果。

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