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A critical view on autoantibodies in lupus nephritis: Concrete knowledge based on evidence 狼疮肾炎自身抗体的批判性观点:基于证据的具体知识。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-27 DOI: 10.1016/j.autrev.2024.103535
Maurizio Bruschi , Andrea Angeletti , Marco Prunotto , Pier Luigi Meroni , Gian Marco Ghiggeri , for the Zeus consortium, Gabriella Moroni , Renato Alberto Sinico , Franco Franceschini , Micaela Fredi , Augusto Vaglio , Andrea Cavalli , Leonardo Scapozza , Jigar J. Patel , John C. Tan , Ken C. Lo , Lorenzo Cavagna , Andrea Petretto , Federico Pratesi , Paola Migliorini , Enrico Verrina

Deposition of autoantibodies in glomeruli is a key factor in the development of lupus nephritis (LN). For a long time, anti-dsDNA and anti-C1q antibodies were thought to be the main cause of the kidney damage. However, recent studies have shown that the list of autoantibidies that have renal tropism and deposit in the kidney in LN is increasing and the link between anti-dsDNA and renal pathology is weak due to potential confounders. Aspecific bindings of dsDNA with cationic antibodies and of anti-dsDNA with several renal antigens such as actinin, laminin, entactin, and annexinA2 raised doubts about the specific target of these antibodies in the kidney. Moreover, the isotype of anti-dsDNA in SLE and LN has never received adequate interest until the recent observation that IgG2 are preponderant over IgG1, IgG3 and IgG4.

Based on the above background, recent studies investigated the involvement of anti-dsDNA IgG2 and of other antibodies in LN. It was concluded that circulating anti-dsDNA IgG2 levels do not distinguish between LN versus non-renal SLE, and, in patients with LN, their levels do not change over time. Circulating levels of other antibodies such as anti-ENO1 and anti-H2 IgG2 were, instead, higher in LN vs non-renal SLE at the time of diagnosis and decreased following therapies. Finally, new classes of renal antibodies that potentially modify the anti-inflammatory response in the kidney are emerging as new co-actors in the pathogenetic scenario. They have been defined as ‘second wave antibodies’ for the link with detoxifying mechanisms limiting the oxidative stress in glomeruli that are classically stimulated in a second phase of inflammation.

These findings have important clinical implications that may modify the laboratory approach to LN. Serum levels of anti-ENO1 and anti-H2 IgG2 should be measured in the follow up of patients for designing the length of therapies and identify those patients who respond to treatments. Anti-SOD2 could help to monitor and potentiate the anti-inflammatory response in the kidney.

自身抗体在肾小球的沉积是狼疮肾炎(LN)发病的关键因素。长期以来,抗dsDNA和抗C1q抗体被认为是肾脏损伤的主要原因。然而,最近的研究表明,在狼疮性肾炎患者中,具有肾脏滋养特性并沉积于肾脏的自身抗体越来越多,而由于潜在的混杂因素,抗dsDNA与肾脏病理之间的联系很弱。dsDNA与阳离子抗体的特异性结合,以及抗dsDNA与多种肾脏抗原(如肌动蛋白、层粘连蛋白、entactin和annexinA2)的特异性结合,使人对这些抗体在肾脏中的特异性靶点产生怀疑。此外,系统性红斑狼疮和 LN 中抗dsDNA 的同种型一直没有引起足够的重视,直到最近发现 IgG2 比 IgG1、IgG3 和 IgG4 占优势。基于上述背景,最近的研究调查了抗dsDNA IgG2和其他抗体在LN中的参与情况。研究得出的结论是,循环中的抗dsDNA IgG2水平并不能区分LN和非肾性系统性红斑狼疮,而且在LN患者中,其水平不会随着时间的推移而改变。相反,其他抗体如抗ENO1和抗H2 IgG2的循环水平在LN和非肾性系统性红斑狼疮诊断时较高,在接受治疗后下降。最后,有可能改变肾脏抗炎反应的新型肾脏抗体正在成为新的致病因素。它们被定义为 "第二波抗体",因为它们与限制肾小球氧化应激的解毒机制有联系,而这种机制在炎症的第二阶段通常会受到刺激。这些发现具有重要的临床意义,可能会改变实验室检测 LN 的方法。在对患者进行随访时,应测量血清中抗 ENO1 和抗 H2 IgG2 的水平,以设计治疗时间的长短,并确定对治疗有反应的患者。抗 SOD2 有助于监测和增强肾脏的抗炎反应。
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引用次数: 0
Redox mechanisms in autoimmune thyroid eye disease 自身免疫性甲状腺眼病的氧化还原机制
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-26 DOI: 10.1016/j.autrev.2024.103534
Francesco Buonfiglio , Katharina A. Ponto , Norbert Pfeiffer , George J. Kahaly , Adrian Gericke

Thyroid eye disease (TED) is an autoimmune condition affecting the orbit and the eye with its adnexa, often occurring as an extrathyroidal complication of Graves' disease (GD). Orbital inflammatory infiltration and the stimulation of orbital fibroblasts, triggering de novo adipogenesis, an overproduction of hyaluronan, myofibroblast differentiation, and eventual tissue fibrosis are hallmarks of the disease. Notably, several redox signaling pathways have been shown to intensify inflammation and to promote adipogenesis, myofibroblast differentiation, and fibrogenesis by upregulating potent cytokines, such as interleukin (IL)-1β, IL-6, and transforming growth factor (TGF)-β. While existing treatment options can manage symptoms and potentially halt disease progression, they come with drawbacks such as relapses, side effects, and chronic adverse effects on the optic nerve. Currently, several studies shed light on the pathogenetic contributions of emerging factors within immunological cascades and chronic oxidative stress. This review article provides an overview on the latest advancements in understanding the pathophysiology of TED, with a special focus of the interplay between oxidative stress, immunological mechanisms and environmental factors. Furthermore, cutting-edge therapeutic approaches targeting redox mechanisms will be presented and discussed.

甲状腺眼病(TED)是一种影响眼眶和眼球及其附件的自身免疫性疾病,通常是巴塞杜氏病(GD)的甲状腺外并发症。眼眶炎症浸润、刺激眼眶成纤维细胞、引发新生脂肪生成、透明质酸过度产生、肌成纤维细胞分化以及最终的组织纤维化是该病的特征。值得注意的是,一些氧化还原信号通路已被证明会加剧炎症,并通过上调白细胞介素(IL)-1β、IL-6 和转化生长因子(TGF)-β 等强效细胞因子促进脂肪生成、肌成纤维细胞分化和纤维化。虽然现有的治疗方案可以控制症状,并有可能阻止疾病的发展,但它们也存在复发、副作用和对视神经的慢性不良影响等缺点。目前,一些研究揭示了免疫级联和慢性氧化应激中新出现因素的致病作用。这篇综述文章概述了在了解 TED 病理生理学方面的最新进展,特别关注氧化应激、免疫机制和环境因素之间的相互作用。此外,文章还将介绍和讨论针对氧化还原机制的前沿治疗方法。
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引用次数: 0
The management of patients with inflammatory bowel disease-associated spondyloarthritis: Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD) and Italian Society of Rheumatology (SIR) recommendations based on a pseudo-Delphi consensus 炎症性肠病相关脊柱关节炎患者的治疗:意大利炎症性肠病研究小组(IG-IBD)和意大利风湿病学会(SIR)根据伪德尔菲共识提出的建议。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-22 DOI: 10.1016/j.autrev.2024.103533
Fabio Salvatore Macaluso , Flavio Caprioli , Laura Benedan , Cristina Bezzio , Roberto Caporali , Alberto Cauli , Maria Sole Chimenti , Francesco Ciccia , Salvatore D'Angelo , Massimo Claudio Fantini , Stefano Festa , Florenzo Iannone , Ennio Lubrano , Paolo Mariani , Claudio Papi , Giuseppe Provenzano , Daniela Pugliese , Antonio Rispo , Simone Saibeni , Carlo Salvarani , Roberto Gerli

Spondyloarthritis (SpA) is the most frequent extraintestinal manifestation in patients with inflammatory bowel diseases (IBD). When IBD and spondyloarthritis coexist, musculoskeletal and intestinal disease features should be considered when planning a therapeutic strategy. Treatment options for IBD and SpA have expanded enormously over the last few years, but randomized controlled trials with specific endpoints focused on SpA are not available in the IBD setting. To address this important clinical topic, the Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD) and the Italian Society of Rheumatology (SIR) jointly planned to draw updated therapeutic recommendations for IBD-associated SpA using a pseudo-Delphi method. This document presents the official recommendations of IG-IBD and SIR on the management of IBD-associated SpA in the form of 34 statements and 4 therapeutic algorithms. It is intended to be a reference guide for gastroenterologists and rheumatologists dealing with IBD-associated SpA.

脊柱关节炎(Spondyloarthritis,SPA)是炎症性肠病(IBD)患者最常见的肠外表现。当 IBD 和脊柱关节炎同时存在时,在制定治疗策略时应考虑肌肉骨骼和肠道疾病的特征。在过去几年中,IBD 和脊柱关节炎的治疗方案有了很大的扩展,但在 IBD 环境中,还没有针对脊柱关节炎的特定终点的随机对照试验。为了解决这一重要的临床课题,意大利炎症性肠病研究小组(IG-IBD)和意大利风湿病学会(SIR)共同计划采用伪德尔菲法,为 IBD 相关性 SpA 制定最新的治疗建议。本文件以 34 项声明和 4 种治疗算法的形式,介绍了 IG-IBD 和 SIR 对 IBD 相关性 SpA 治疗的官方建议。它旨在为消化内科医生和风湿病学家处理 IBD 相关性 SpA 提供参考指南。
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引用次数: 0
Inhibitors of Bruton's tyrosine kinase as emerging therapeutic strategy in autoimmune diseases 布鲁顿酪氨酸激酶抑制剂作为自身免疫性疾病的新兴治疗策略。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-22 DOI: 10.1016/j.autrev.2024.103532
Mirre De Bondt , Janne Renders , Sofie Struyf , Niels Hellings

Bruton's tyrosine kinase (BTK) is a cytoplasmic, non-receptor signal transducer, initially identified as an essential signaling molecule for B cells, with genetic mutations resulting in a disorder characterized by disturbed B cell and antibody development. Subsequent research revealed the critical role of BTK in the functionality of monocytes, macrophages and neutrophils. Various immune cells, among which B cells and neutrophils, rely on BTK activity for diverse signaling pathways downstream of multiple receptors, which makes this kinase an ideal target to treat hematological malignancies and autoimmune diseases. First-generation BTK inhibitors are already on the market to treat hematological disorders. It has been demonstrated that B cells and myeloid cells play a significant role in the pathogenesis of different autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus and primary Sjögren's syndrome. Consequently, second-generation BTK inhibitors are currently being developed to treat these disorders. Despite the acknowledged involvement of BTK in various cell types, the focus on B cells often overshadows its impact on innate immune cells. Among these cell types, neutrophils are often underestimated in the pathogenesis of autoimmune diseases. In this narrative review, the function of BTK in different immune cell subsets is discussed, after which an overview is provided of different upcoming BTK inhibitors tested for treatment of autoimmune diseases. Special attention is paid to BTK inhibition and its effect on neutrophil biology.

布鲁顿酪氨酸激酶(BTK)是一种细胞质非受体信号转换器,最初被认为是 B 细胞的重要信号分子,基因突变导致 B 细胞和抗体发育紊乱。随后的研究发现,BTK 对单核细胞、巨噬细胞和中性粒细胞的功能起着关键作用。各种免疫细胞,包括 B 细胞和中性粒细胞,都依赖 BTK 的活性来实现多种受体下游的信号通路,这使得这种激酶成为治疗血液恶性肿瘤和自身免疫性疾病的理想靶点。第一代 BTK 抑制剂已经上市,用于治疗血液病。研究表明,B 细胞和骨髓细胞在多发性硬化症、类风湿性关节炎、系统性红斑狼疮和原发性斯约格伦综合征等不同自身免疫性疾病的发病机制中起着重要作用。因此,目前正在开发第二代 BTK 抑制剂来治疗这些疾病。尽管 BTK 参与各种细胞类型的研究已得到公认,但对 B 细胞的关注往往掩盖了它对先天性免疫细胞的影响。在这些细胞类型中,中性粒细胞在自身免疫性疾病发病机制中的作用往往被低估。在这篇叙述性综述中,讨论了 BTK 在不同免疫细胞亚群中的功能,然后概述了即将测试用于治疗自身免疫性疾病的各种 BTK 抑制剂。其中特别关注 BTK 抑制及其对中性粒细胞生物学的影响。
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引用次数: 0
Formation and clinical effects of anti-drug antibodies against biologics in psoriasis treatment: An analysis of current evidence 银屑病治疗中针对生物制剂的抗药性抗体的形成和临床效果:现有证据分析。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-17 DOI: 10.1016/j.autrev.2024.103530
Xiaoying Sun , Ziyang Cui , Qingyun Wang , Liu Liu , Xiaojie Ding , Jiao Wang , Xiaoce Cai , Bin Li , Xin Li

Background

Formation of anti-drug antibodies (ADAs) against biologics is an important cause of psoriasis treatment failure.

Objective

This study aimed to summarize the characteristics of ADAs formation under different biological therapies and the influence of ADAs on the clinical effects and safety of biologics in patients with psoriasis.

Methods

PubMed, Embase, and Web of Science databases were searched from their inception to August 2022. Studies on biologics that assessed ADA levels in patients with psoriasis were included. The Cochrane risk-of-bias tool was used to assess the quality of randomized controlled trials (RCTs), the Newcastle-Ottawa Quality Assessment Scale (NOS) for case-control and cohort studies, and the Joanna Briggs Institute (JBI) critical appraisal checklist for single-arm studies. We calculated the pooled incidence with a random-effects model using R software. Subgroup analyses revealed that differences in patient characteristics, disease conditions, study design, and immunoassays may influence ADA generation and detection.

Results

The analysis included 86 studies, with a total population of 42,280 individuals. The pooled ADA rates were 0.49%, 2.20%, 2.38%, 4.08%, 7.38%, 7.94%, 14.29%, 21.93%, 29.70%, 31.76%, and 39.58% for secukinumab, etanercept, brodalumab, ustekinumab, tildrakizumab, guselkumab, ixekizumab, risankizumab, infliximab, adalimumab, and bimekizumab, respectively. >70% (95% CI, 0.71–0.81) of ADAs against adalimumab were neutralizing antibodies, and over 70% of ADAs against secukinumab and brodalumab were transient. Concomitant methotrexate therapy with tumor necrosis factor-α (TNF-α) inhibitors decreased ADA levels. Lower infliximab doses and intermittent therapy with interleukin (IL)-23 p19 inhibitors increased ADA formation. Additionally, ADA formation under treatment using TNF-α inhibitors and IL-12/23 p40 inhibitors was associated with lower response rates or serum drug levels, but only high ADA titers reduced the clinical effects of IL-17 inhibitors. The occurrence of IL-23 p19 and TNF-α inhibitors has been linked to injection-site reactions.

Conclusions

Among the 11 biologics, secukinumab, etanercept, and brodalumab resulted in the lowest ADA formation rates. Immunogenicity contributes to lower biological efficacy and a higher likelihood of injection-site reactions. Low doses, intermittent treatment may increase ADA formation. An appropriate biologic should be selected based on the ADA formation rate and course of treatment.

背景:针对生物制剂的抗药性抗体(ADA)的形成是牛皮癣治疗失败的重要原因:针对生物制剂的抗药抗体(ADA)的形成是银屑病治疗失败的重要原因:本研究旨在总结不同生物疗法下ADA形成的特点,以及ADA对银屑病患者使用生物制剂的临床效果和安全性的影响:方法:对 PubMed、Embase 和 Web of Science 数据库从开始到 2022 年 8 月的内容进行了检索。纳入了评估银屑病患者体内 ADA 水平的生物制剂研究。科克伦偏倚风险工具用于评估随机对照试验(RCT)的质量,纽卡斯尔-渥太华质量评估量表(NOS)用于病例对照和队列研究,乔安娜-布里格斯研究所(JBI)关键评估清单用于单臂研究。我们使用 R 软件的随机效应模型计算了汇总发病率。亚组分析表明,患者特征、疾病状况、研究设计和免疫测定方法的不同可能会影响ADA的产生和检测:分析包括 86 项研究,总人数为 42,280 人。secukinumab、etanercept、brodalumab、ustekinumab、tildrakizumab、guselkumab、ixekizumab、risankizumab、infliximab、adalimumab和bimekizumab的合并ADA率分别为0.49%、2.20%、2.38%、4.08%、7.38%、7.94%、14.29%、21.93%、29.70%、31.76%和39.58%。针对阿达木单抗的ADA中>70%(95% CI,0.71-0.81)为中和抗体,针对secukinumab和brodalumab的ADA中超过70%为一过性抗体。甲氨蝶呤与肿瘤坏死因子-α(TNF-α)抑制剂同时治疗会降低ADA水平。较低的英夫利西单抗剂量和白细胞介素(IL)-23 p19抑制剂的间歇治疗会增加ADA的形成。此外,在使用TNF-α抑制剂和IL-12/23 p40抑制剂治疗时,ADA的形成与较低的应答率或血清药物水平有关,但只有高ADA滴度才会降低IL-17抑制剂的临床效果。IL-23 p19和TNF-α抑制剂的发生与注射部位反应有关:在11种生物制剂中,secukinumab、etanercept和brodalumab的ADA形成率最低。免疫原性会降低生物疗效,增加注射部位反应的可能性。小剂量、间歇性治疗可能会增加 ADA 的形成。应根据 ADA 形成率和疗程选择合适的生物制剂。
{"title":"Formation and clinical effects of anti-drug antibodies against biologics in psoriasis treatment: An analysis of current evidence","authors":"Xiaoying Sun ,&nbsp;Ziyang Cui ,&nbsp;Qingyun Wang ,&nbsp;Liu Liu ,&nbsp;Xiaojie Ding ,&nbsp;Jiao Wang ,&nbsp;Xiaoce Cai ,&nbsp;Bin Li ,&nbsp;Xin Li","doi":"10.1016/j.autrev.2024.103530","DOIUrl":"10.1016/j.autrev.2024.103530","url":null,"abstract":"<div><h3>Background</h3><p>Formation of anti-drug antibodies (ADAs) against biologics is an important cause of psoriasis treatment failure.</p></div><div><h3>Objective</h3><p>This study aimed to summarize the characteristics of ADAs formation under different biological therapies and the influence of ADAs on the clinical effects and safety of biologics in patients with psoriasis.</p></div><div><h3>Methods</h3><p>PubMed, Embase, and Web of Science databases were searched from their inception to August 2022. Studies on biologics that assessed ADA levels in patients with psoriasis were included. The Cochrane risk-of-bias tool was used to assess the quality of randomized controlled trials (RCTs), the Newcastle-Ottawa Quality Assessment Scale (NOS) for case-control and cohort studies, and the Joanna Briggs Institute (JBI) critical appraisal checklist for single-arm studies. We calculated the pooled incidence with a random-effects model using R software. Subgroup analyses revealed that differences in patient characteristics, disease conditions, study design, and immunoassays may influence ADA generation and detection.</p></div><div><h3>Results</h3><p>The analysis included 86 studies, with a total population of 42,280 individuals. The pooled ADA rates were 0.49%, 2.20%, 2.38%, 4.08%, 7.38%, 7.94%, 14.29%, 21.93%, 29.70%, 31.76%, and 39.58% for secukinumab, etanercept, brodalumab, ustekinumab, tildrakizumab, guselkumab, ixekizumab, risankizumab, infliximab, adalimumab, and bimekizumab, respectively. &gt;70% (95% CI, 0.71–0.81) of ADAs against adalimumab were neutralizing antibodies, and over 70% of ADAs against secukinumab and brodalumab were transient. Concomitant methotrexate therapy with tumor necrosis factor-α (TNF-α) inhibitors decreased ADA levels. Lower infliximab doses and intermittent therapy with interleukin (IL)-23 p19 inhibitors increased ADA formation. Additionally, ADA formation under treatment using TNF-α inhibitors and IL-12/23 p40 inhibitors was associated with lower response rates or serum drug levels, but only high ADA titers reduced the clinical effects of IL-17 inhibitors. The occurrence of IL-23 p19 and TNF-α inhibitors has been linked to injection-site reactions.</p></div><div><h3>Conclusions</h3><p>Among the 11 biologics, secukinumab, etanercept, and brodalumab resulted in the lowest ADA formation rates. Immunogenicity contributes to lower biological efficacy and a higher likelihood of injection-site reactions. Low doses, intermittent treatment may increase ADA formation. An appropriate biologic should be selected based on the ADA formation rate and course of treatment.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 4","pages":"Article 103530"},"PeriodicalIF":13.6,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140157509","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
Epidemiology, clinical features, risk factors, and outcomes in anti-glomerular basement membrane disease: A systematic review and meta-analysis 抗肾小球基底膜病的流行病学、临床特征、风险因素和预后:系统回顾与荟萃分析。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-16 DOI: 10.1016/j.autrev.2024.103531
Huang Kuang , Nan Jiang , Xiao-Yu Jia , Zhao Cui , Ming-Hui Zhao

Anti-glomerular basement membrane (GBM) disease is a small-vessel vasculitis that represents the most aggressive form of autoimmune glomerulonephritis. The study aimed to investigate the prevalence, clinical characteristics, risk factors, and outcomes of anti-GBM disease through a systematic review and meta-analysis involving 47 studies with 2830 patients. The overall incidence of anti-GBM disease ranged from 0.60 to 1.79 per million population per annum. In rapidly progressive glomerulonephritis and crescentic glomerulonephritis, the pooled incidence rates were 8.0% and 12.8%, respectively. The pooled prevalence rates of anti-GBM antibodies, antineutrophil cytoplasmic antibodies (ANCA), and lung hemorrhage were 88.8%, 27.4%, and 32.6%, respectively. Patients with combined ANCA positivity demonstrated a prognosis comparable to those patients with only anti-GBM antibodies, though with differing clinical features. The pooled one-year patient and kidney survival rates were 76.2% and 30.2%, respectively. Kidney function on diagnosis and normal glomeruli percentage were identified as strong prognostic factors. This study represents the first comprehensive meta-analysis on anti-GBM disease, providing insights into its management. However, caution is warranted in interpreting some results due to the observational nature of the included studies and high heterogeneity.

抗肾小球基底膜病(GBM)是一种小血管炎,是自身免疫性肾小球肾炎中最具侵袭性的一种。该研究旨在通过一项系统性回顾和荟萃分析,调查抗肾小球基底膜病的发病率、临床特征、风险因素和预后,共涉及 47 项研究,2830 名患者。抗 GBM 疾病的总体发病率为每年每百万人口 0.60 至 1.79 例。在快速进展性肾小球肾炎和新月体性肾小球肾炎中,汇总发病率分别为 8.0% 和 12.8%。抗 GBM 抗体、抗中性粒细胞胞浆抗体(ANCA)和肺出血的汇总发病率分别为 88.8%、27.4% 和 32.6%。合并 ANCA 阳性的患者的预后与仅有抗 GBM 抗体的患者相当,但临床特征有所不同。患者和肾脏的一年存活率分别为76.2%和30.2%。诊断时的肾功能和正常肾小球百分比被认为是强有力的预后因素。这项研究是首次对抗 GBM 疾病进行全面的荟萃分析,为其治疗提供了启示。然而,由于纳入研究的观察性质和高度异质性,在解释某些结果时需要谨慎。
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引用次数: 0
Cerebral vasculitis as a clinical manifestation of neurosarcoidosis: A scoping review 作为神经肉芽肿病临床表现的脑血管炎:范围综述。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-16 DOI: 10.1016/j.autrev.2024.103528
Yaroslav Winter , Sergiu Groppa , Timo Uphaus , Erik Ellwardt , Sven Fuest , Sven Meuth , Stefan Bittner , Eyad Hayani

The occurrence of cerebral vasculitis in individuals with neurosarcoidosis (NS) is considered to be rare. Although the number of relevant publications has increased in recent years, evidence is mostly limited to case reports. To obtain a better understanding of this rare and severe manifestation of disease, we carried out a scoping review on cerebral vasculitis in patients diagnosed with NS. The results of the review indicate that the diagnosis of cerebral vasculitis in patients with NS is made especially in patients with systemic sarcoidosis. However, recurrent strokes in patients with NS remains the main indicator of cerebral vasculitis. A tissue biopsy is considered the gold standard to confirm the diagnosis despite occasional false-negative results. Glucocorticoids and steroid-sparing agents are the most successful current treatments. Favorable outcomes were observed with strategies targeting TNFα and B cells. The goal of this review is to summarize the current literature and treatment options for cerebral vasculitis in patients with NS.

神经肉芽肿病(NS)患者发生脑血管炎被认为是罕见的。尽管近年来相关文献的数量有所增加,但证据大多仅限于病例报告。为了更好地了解这种罕见而严重的疾病表现,我们对确诊为神经肉芽肿病(NS)患者的脑血管炎进行了一次范围界定综述。综述结果表明,NS 患者中脑血管炎的诊断尤其适用于全身性肉样瘤病患者。然而,NS 患者反复中风仍是脑血管炎的主要指标。组织活检被认为是确诊的金标准,尽管有时会出现假阴性结果。糖皮质激素和节省类固醇的药物是目前最成功的治疗方法。针对 TNFα 和 B 细胞的治疗策略也取得了良好的疗效。本综述旨在总结目前的文献和治疗NS患者脑血管炎的方案。
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引用次数: 0
Structural cell heterogeneity underlies the differential contribution of IL-17A, IL-17F and IL-23 to joint versus skin chronic inflammation IL-17A、IL-17F 和 IL-23 对关节和皮肤慢性炎症的不同贡献是结构细胞异质性的基础。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-15 DOI: 10.1016/j.autrev.2024.103529
Marie Robert, Pierre Miossec

The current therapeutic strategy used in immune-mediated inflammatory diseases (IMIDs) primarily targets immune cells or associated-pathways. However, recent evidence suggests that the microenvironment modulates immune cell development and responses. During inflammation, structural cells acquire a pathogenetic phenotype and the interactions with immune cells are often greatly modified. Understanding the importance of these tissue-specific interactions may allow to explain why some biologics are effective in some IMIDs but not in others. The differential effects of interleukin (IL)-17 A, IL-17F and IL-23 in joint versus skin inflammation depends on structural cell heterogeneity. In addition, the sometimes opposite effects of immune/structural cell interactions on the production of these cytokines illustrate the importance of these cells in chronic inflammation, using the examples of rheumatoid arthritis, psoriasis and spondyloarthritis. This review describes these concepts, shows their interests through clinical observations, and finally discusses strategies to optimize therapeutic strategies.

目前用于免疫介导的炎症性疾病(IMIDs)的治疗策略主要针对免疫细胞或相关途径。然而,最近的证据表明,微环境会调节免疫细胞的发育和反应。在炎症过程中,结构细胞会获得致病表型,与免疫细胞的相互作用通常会发生很大变化。了解了这些组织特异性相互作用的重要性,就可以解释为什么一些生物制剂对某些 IMIDs 有效,而对另一些则无效。白细胞介素(IL)-17 A、IL-17F 和 IL-23 在关节炎症和皮肤炎症中的不同作用取决于结构细胞的异质性。此外,以类风湿性关节炎、银屑病和脊柱关节炎为例,免疫/结构细胞相互作用对这些细胞因子的产生有时会产生相反的影响,这说明了这些细胞在慢性炎症中的重要性。这篇综述描述了这些概念,通过临床观察说明了它们的重要性,最后讨论了优化治疗策略的策略。
{"title":"Structural cell heterogeneity underlies the differential contribution of IL-17A, IL-17F and IL-23 to joint versus skin chronic inflammation","authors":"Marie Robert,&nbsp;Pierre Miossec","doi":"10.1016/j.autrev.2024.103529","DOIUrl":"10.1016/j.autrev.2024.103529","url":null,"abstract":"<div><p>The current therapeutic strategy used in immune-mediated inflammatory diseases (IMIDs) primarily targets immune cells or associated-pathways. However, recent evidence suggests that the microenvironment modulates immune cell development and responses. During inflammation, structural cells acquire a pathogenetic phenotype and the interactions with immune cells are often greatly modified. Understanding the importance of these tissue-specific interactions may allow to explain why some biologics are effective in some IMIDs but not in others. The differential effects of interleukin (IL)-17 A, IL-17F and IL-23 in joint versus skin inflammation depends on structural cell heterogeneity. In addition, the sometimes opposite effects of immune/structural cell interactions on the production of these cytokines illustrate the importance of these cells in chronic inflammation, using the examples of rheumatoid arthritis, psoriasis and spondyloarthritis. This review describes these concepts, shows their interests through clinical observations, and finally discusses strategies to optimize therapeutic strategies.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 4","pages":"Article 103529"},"PeriodicalIF":13.6,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140139793","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
Clinical phenotype of AAV, anti-GBM disease and double-positive patients after SARS-CoV-2 vaccination 接种 SARS-CoV-2 疫苗后 AAV、抗 GBM 疾病和双阳性患者的临床表型。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-13 DOI: 10.1016/j.autrev.2024.103521
Yisha Li , Jie Wang , Shuang Liang, Yan Zhang, Zhe Feng, Guangyan Cai

The number of anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV), anti-glomerular basement membrane (GBM) disease and double-positive patients (DPPs) following the coronavirus disease 2019 (COVID-19) vaccine reported in the literature is increasing, we reviewed the reported cases of AAV, anti-GBM disease and DPPs subsequent to COVID-19 vaccination, and compared the disparities in DPPs who received the COVID-19 vaccination and those who did not. We did not observe any differences in clinical phenotype of AAV, anti-GBM disease and DPPs before and after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination.

文献中报道的接种冠状病毒病2019(COVID-19)疫苗后出现抗中性粒细胞胞浆抗体(ANCA)相关性血管炎(AAV)、抗肾小球基底膜(GBM)病和双阳性患者(DPPs)的数量正在增加,我们回顾了接种COVID-19疫苗后出现AAV、抗GBM病和DPPs的报道病例,并比较了接种COVID-19疫苗和未接种COVID-19疫苗的DPPs的差异。我们没有观察到接种严重急性呼吸系统综合症冠状病毒 2(SARS-CoV-2)疫苗前后 AAV、抗 GBM 病和 DPP 的临床表型有任何差异。
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引用次数: 0
Ethnicity also influences the clinical heterogeneity of mixed connective tissue disease of childhood onset: The French West Indies experience 种族也会影响儿童期混合性结缔组织病的临床异质性:法属西印度群岛的经验。
IF 13.6 1区 医学 Q1 IMMUNOLOGY Pub Date : 2024-03-05 DOI: 10.1016/j.autrev.2024.103519
Arthur Felix , Fabienne Louis-Sidney , Christophe Deligny , Benoit Suzon
{"title":"Ethnicity also influences the clinical heterogeneity of mixed connective tissue disease of childhood onset: The French West Indies experience","authors":"Arthur Felix ,&nbsp;Fabienne Louis-Sidney ,&nbsp;Christophe Deligny ,&nbsp;Benoit Suzon","doi":"10.1016/j.autrev.2024.103519","DOIUrl":"10.1016/j.autrev.2024.103519","url":null,"abstract":"","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 4","pages":"Article 103519"},"PeriodicalIF":13.6,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140048651","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
期刊
Autoimmunity reviews
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