Autoimmunity reviews最新文献_第10页

Combination targeted therapy with two biologic/targeted synthetic DMARDs in 1200 patients with immune mediated inflammatory diseases. A systematic literature review for current landscape in safety and efficacy 两种生物/靶向合成dmard联合靶向治疗1200例免疫介导炎性疾病患者对安全性和有效性的现状进行系统的文献综述。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-07-07 DOI: 10.1016/j.autrev.2025.103865

Angeliki Zoi Lignou , Konstantinos D. Vassilakis , Xenofon Baraliakos , Petros P. Sfikakis , Jacques-Eric Gottenberg , George E. Fragoulis

Background

Immune-mediated inflammatory diseases (IMID) include rheumatoid arthritis (RA), psoriatic arthritis (PsA), axial spondyloarthritis (axSpA), Crohn's disease (CD), ulcerative colitis (UC), and psoriasis (PsO). While biologic (b) and targeted synthetic (ts) DMARDs are effective, nearly 60 % of patients fail to achieve low disease activity status. Combination targeted therapy (CTT) using concomitantly two different b- or ts-DMARDs has been explored, but results on safety and efficacy are unclear.

Objective

To systematically review the literature on CTT in IMID.

Methods

Following the PICO framework, we included literature of adult patients (≥18 years) with IMID receiving CTT. Three databases (PubMed, Scopus, Epistemonikos) were searched up to June 2024. Studies in non-English, pediatric populations, and non-approved treatments were excluded. Risk of bias was assessed using approved tools.

Results

Of 2038 records, 70 studies (6 RCTs, 11 cohorts, 22 case series, 31 case reports) involving 1200 patients were analyzed. About 75 % of them demonstrated low risk of bias. The most studied combinations were TNFi+IL/23i, JAKi+bDMARDs, and vedolizumab+TNFi. Approximately 40-60 % of patients with PsA, axSpA, and IBD with refractory disease improved with TNFi+IL/23i CTT. About half of patients with inflammatory arthritis and up to 80 % of IBD cases benefited with JAKi+bDMARD CTT, whereas favorable outcomes were observed in 30-50 % of IBD patients following Vedolizumab+TNFi CTT. Safety profiles were generally acceptable, without emerging signals so far.

Conclusion

CTT benefits about half of refractory IMID patients, particularly TNFi/IL-23i, JAKi/bDMARD, and vedolizumab/TNFi combinations, without raising significant safety issues. Further research is needed to clarify safety and efficacy across diseases.

背景：免疫介导的炎症性疾病（IMID）包括类风湿关节炎（RA）、银屑病关节炎（PsA）、轴性脊柱炎（axSpA）、克罗恩病（CD）、溃疡性结肠炎（UC）和牛皮癣（PsO）。虽然生物制剂(b)和靶向合成（ts） dmard是有效的，但近60% %的患者未能达到低疾病活动状态。联合靶向治疗（CTT）联合使用两种不同的b-或ts- dmard已被探索，但安全性和有效性的结果尚不清楚。目的：系统回顾IMID中CTT的相关文献。方法：根据PICO框架，我们纳入了接受CTT治疗的IMID成年患者（≥18 岁）的文献。检索三个数据库（PubMed, Scopus, Epistemonikos）至2024年6月。非英语、儿科人群和未批准治疗的研究被排除在外。使用经批准的工具评估偏倚风险。结果：在2038份记录中，分析了涉及1200名患者的70项研究（6项随机对照试验，11个队列，22个病例系列，31个病例报告）。其中约75% %表现出低偏倚风险。研究最多的组合是TNFi+IL/23i， JAKi+bDMARDs和vedolizumab+TNFi。大约40- 60% %伴有难治性疾病的PsA、axSpA和IBD患者通过TNFi+IL/23i CTT得到改善。大约一半的炎症性关节炎患者和高达80% %的IBD病例受益于JAKi+bDMARD CTT，而30- 50% %的IBD患者在Vedolizumab+TNFi CTT中观察到良好的结果。安全概况总体上可以接受，到目前为止没有出现信号。结论：CTT使大约一半的难治性IMID患者受益，特别是TNFi/IL-23i， JAKi/bDMARD和vedolizumab/TNFi联合，没有引起明显的安全性问题。需要进一步的研究来澄清跨疾病的安全性和有效性。

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引用次数: 0

Glucagon-Like Peptide-1 (GLP-1) receptor agonists in rheumatology: A review of current evidence and future directions 胰高血糖素样肽-1 （GLP-1）受体激动剂在风湿病学中的应用：当前证据和未来方向的综述。

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-07-03 DOI: 10.1016/j.autrev.2025.103864

Emre Bilgin , Vincenzo Venerito , Dimitrios P. Bogdanos

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have improved the management of type 2 diabetes and obesity. Increasing evidence suggests their potential therapeutic role in rheumatic and musculoskeletal diseases, yet their precise mechanisms and clinical implications remain under investigation. This scoping review evaluates the current evidence on GLP-1 RAs in inflammatory arthritis, osteoarthritis, systemic autoimmune diseases, and other rheumatic conditions. This systematic literature search followed PRISMA-ScR guidelines and identified 52 studies and seven clinical trials from Scopus, PubMed, and ClinicalTrials.gov. Although most of the included studies had a risk of bias, the findings suggest that GLP-1 RAs may influence inflammatory pathways, oxidative stress, and immune regulation in conditions such as rheumatoid arthritis (RA), psoriatic arthritis (PsA), systemic lupus erythematosus (SLE), osteoarthritis (OA), and gout. In RA and PsA, GLP-1 RAs have demonstrated potential disease-modifying effects, reducing inflammatory cytokine expression and improving metabolic parameters; however, their clinical impact remains partially linked to weight loss. Studies on OA indicate chondroprotective and anti-inflammatory properties, yet their effect on disease progression remains inconclusive.

Additionally, GLP-1 RAs have been associated with cardiovascular and renal benefits in SLE, though concerns about autoimmune activation persist. Despite promising findings, several challenges remain, including heterogeneous clinical responses, the need for head-to-head comparisons with standard rheumatologic therapies, and a lack of long-term safety data in autoimmune conditions. Drug-induced autoimmune phenomena, cost considerations, and accessibility limitations must be addressed. Future research should focus on distinguishing between metabolic and direct immunomodulatory effects, optimizing combination therapies, and evaluating safety concerns. GLP-1 RAs hold potential as a novel therapeutic approach in rheumatology, but further well-designed randomized controlled trials are essential to establish their clinical role.

胰高血糖素样肽-1受体激动剂（GLP-1 RAs）改善了2型糖尿病和肥胖的管理。越来越多的证据表明它们在风湿病和肌肉骨骼疾病中具有潜在的治疗作用，但它们的确切机制和临床意义仍在研究中。本综述评估了GLP-1 RAs在炎性关节炎、骨关节炎、系统性自身免疫性疾病和其他风湿病中的现有证据。该系统文献检索遵循PRISMA-ScR指南，并从Scopus、PubMed和ClinicalTrials.gov中确定了52项研究和7项临床试验。尽管大多数纳入的研究都存在偏倚风险，但研究结果表明，GLP-1 RAs可能影响类风湿关节炎（RA）、银屑病关节炎（PsA）、系统性红斑狼疮（SLE）、骨关节炎（OA）和痛风等疾病的炎症途径、氧化应激和免疫调节。在RA和PsA中，GLP-1 RAs已显示出潜在的疾病改善作用，可降低炎症细胞因子表达并改善代谢参数；然而，它们的临床效果仍然部分与减肥有关。研究表明OA具有软骨保护和抗炎特性，但它们对疾病进展的影响仍不确定。此外，GLP-1 RAs与SLE的心血管和肾脏益处有关，尽管对自身免疫激活的担忧仍然存在。尽管有令人鼓舞的发现，但仍存在一些挑战，包括异质临床反应，需要与标准风湿病疗法进行正面比较，以及缺乏自身免疫性疾病的长期安全性数据。必须解决药物引起的自身免疫现象、成本考虑和可及性限制。未来的研究应侧重于区分代谢和直接免疫调节作用，优化联合疗法，并评估安全性问题。GLP-1 RAs具有作为风湿病治疗新方法的潜力，但进一步精心设计的随机对照试验对于确定其临床作用至关重要。

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引用次数: 0

Epidemiological patterns and in-hospital mortality in ANCA-associated vasculitis: Insights from Spain's National Health Data (2016–2022) anca相关血管炎的流行病学模式和住院死亡率：来自西班牙国家健康数据的见解（2016-2022）

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews

Pub Date : 2025-06-30 DOI: 10.1016/j.autrev.2025.103863

Francisco-Josué Cordero-Pérez , Pablo Martínez-Rodríguez , Luis Arribas-Pérez , David Puertas-Miranda , Carlos-Rafael Pires-Baltazar , Leticia Salcedo-Martín , Juan Antonio Sánchez-Villoria , Erik Gabriel Díaz-Ávila , Hugo-Guillermo Ternavasio-De La Vega , Miguel Marcos , Antonio-Javier Chamorro

Background

ANCA-associated vasculitis (AAV), including granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA), is a systemic autoimmune disease. This study represents the first large-scale analysis of AAV hospitalisation rates and in-hospital mortality trends in Spain.

Methods

A retrospective longitudinal analysis of AAV-related hospital admissions between 2016 and 2022 was conducted using the ICD-10 codes from the Minimum Basic Dataset (MBDS) of the Spanish National Health System. Statistical analyses were performed, including odds ratios, Student's t-tests, and Mantel-Haenszel trend tests.

Results

Among 5753 AAV episodes, GPA was the most frequent subtype (53.9 %), followed by MPA (31.5 %) and EGPA (14.6 %). AAV episodes were more frequent in older patients (> 65 years) than in other hospital episodes (62.9 % vs. 38.9 %; OR: 2.66, 95 %CI: 2.51–2.80; P < 0.001). Larger hospitals accounted for more AAV episodes, longer hospital stays, and higher costs. MPA had the highest mortality rate (7.2 % vs. 4.9 %; OR: 1.52, 95 % CI: 1.27–1.79; P < 0.001), particularly in patients over 65 years (83.1 % vs. 61.8 %; OR: 3.04, 95 % CI: 2.47–3.75; P < 0.001) compared with the other AAV. In the GPA group, renal involvement significantly increased mortality compared to GPA cases without renal involvement (6.6 % vs. 4.6 %; OR: 1.46, 95 % CI: 1.16–1.83; P = 0.011). Notably, the relative risk of AAV-related deaths increased over the study period (Z = 2.77, P < 0.01).

Conclusion

AAV, particularly MPA, is associated with increased hospital mortality, particularly among older adults and patients with renal involvement.

anca相关性血管炎（AAV），包括肉芽肿病合并多血管炎（GPA）、显微多血管炎（MPA）和嗜酸性肉芽肿病合并多血管炎（EGPA），是一种全身性自身免疫性疾病。该研究首次对西班牙AAV住院率和住院死亡率趋势进行了大规模分析。方法采用西班牙国家卫生系统最低基本数据集（MBDS）的ICD-10代码，对2016 - 2022年aav相关住院病例进行回顾性纵向分析。进行统计分析，包括优势比、学生t检验和Mantel-Haenszel趋势检验。结果5753例AAV发作中，GPA亚型最多（53.9%），MPA亚型次之（31.5%），EGPA亚型次之（14.6%）。AAV发作在老年患者中更为频繁(>；65岁)比其他医院发作(62.9%对38.9%；Or: 2.66, 95% ci: 2.51-2.80；P & lt;0.001)。大型医院的AAV发作次数更多，住院时间更长，费用更高。MPA的死亡率最高(7.2% vs. 4.9%；Or: 1.52, 95% ci: 1.27-1.79；P & lt;0.001)，尤其是65岁以上的患者(83.1% vs. 61.8%；Or: 3.04, 95% ci: 2.47-3.75；P & lt;0.001)，与其他AAV相比。在GPA组中，与没有肾脏受累的GPA患者相比，肾脏受累的死亡率显著增加(6.6% vs. 4.6%；Or: 1.46, 95% ci: 1.16-1.83；p = 0.011)。值得注意的是，在研究期间，aav相关死亡的相对风险增加(Z = 2.77, P <；0.01)。结论：aav，特别是MPA，与医院死亡率增加有关，特别是在老年人和肾脏受累患者中。

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引用次数: 0

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。

{"title":"The efficacy and safety of monoclonal anti-TNF antibodies in the treatment of vascular Behçet's syndrome: A systematic review and meta-analysis","authors":"Yeling Liu , Jingwen Wu , Yiyuan Ao , Lu Li , Xiaoou Wang , Menghao Zhang , Xin Yu , Luxi Sun , Jinjing Liu , Wenjie Zheng","doi":"10.1016/j.autrev.2025.103862","DOIUrl":"10.1016/j.autrev.2025.103862","url":null,"abstract":"<div><h3>Objectives</h3><div>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).</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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 % (<em>n</em> = 12) experienced a relapse. Adverse events (AEs) were reported in 10 studies involving 42 patients, with 31 patients experiencing severe AEs, including 5 deaths.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 9","pages":"Article 103862"},"PeriodicalIF":9.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144551824","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

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