首页 > 最新文献

Autoimmunity reviews最新文献

英文 中文
Impact of GLP-1 analogues on immune-mediated inflammatory diseases: A systematic review GLP-1类似物对免疫介导炎性疾病的影响:系统综述
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103936
Chhagan L. Birda , Fadwa Ibrahim , Abhirup Chatterjee , Anuraag Jena , Vishal Sharma , Shaji Sebastian

Objective

Glucagon-like peptide-1 receptor agonists (GLP1RA) are believed to have anti-inflammatory properties apart from antidiabetic and anti-obesity effects.

Methods

We performed a systematic review to evaluate the efficacy and safety of GLP1RA in immune-mediated inflammatory disorders (IMIDs). A systematic search was done on 3rd April 2025 in PubMed, Scopus, and Embase for studies reporting the use of GLP1RA among patients with IMIDs. Because of significant heterogeneity and overlapping data originating from the same insurance databases, we decided against performing a data synthesis and meta-analysis. We summarised the data regarding clinical and metabolic outcomes in patients with IMIDs with/without the use of GLP1RA.

Results

Thirty-three studies (20 full text, 13 conference abstracts) were included, of which 20 studies focused on inflammatory bowel disease (IBD) and 13 on other IMIDs. Of the three studies reporting on new onset IBD/IMID in GLP1RA users, 2 showed a lower incidence. IBD therapy utilization was reported in 13 studies; steroid use was lower in 5 studies, but the data on the use of biologics were inconclusive. Other outcomes, like hospitalization, IBD complications, surgery, and mortality, seemed to be better in GLP1RA cohorts in a few of the studies. Similarly, psoriasis disease activity-related outcomes were better in the GLP1RA cohort, but the effect on other IMIDs was limited by sparse literature. A total of 12 studies reported metabolic outcomes, including weight loss, glycaemic control, waist circumference, and lipid parameters, all of which showed beneficial effects of GLP1RAs, and these results were comparable to non-IBD/IMID controls. Adverse events (AEs) were reported by 13 studies; gastrointestinal (GI) AEs were higher in the GLP1RA cohort (but the majority were non-severe).

Conclusion

GLP1RA use is associated with better disease activity and metabolic outcomes in patients with IMIDs and concomitant metabolic disorders.
Registration: https://osf.io/jvmz6
目的:胰高血糖素样肽-1受体激动剂(GLP1RA)被认为除具有抗糖尿病和抗肥胖作用外,还具有抗炎作用。方法:我们对GLP1RA治疗免疫介导炎性疾病(IMIDs)的疗效和安全性进行了系统评价。我们于2025年4月3日在PubMed、Scopus和Embase中进行了系统检索,以报告在IMIDs患者中使用GLP1RA的研究。由于来自相同保险数据库的显著异质性和重叠数据,我们决定不进行数据综合和荟萃分析。我们总结了使用/不使用GLP1RA的IMIDs患者的临床和代谢结果的数据。结果:纳入33项研究(20篇全文,13篇会议摘要),其中20项研究关注炎症性肠病(IBD), 13项研究关注其他IMIDs。在报告GLP1RA使用者新发IBD/IMID的三项研究中,2项研究显示发病率较低。13项研究报告了IBD治疗的使用情况;在5项研究中,类固醇的使用较低,但关于生物制剂使用的数据尚无定论。在一些研究中,GLP1RA组的其他结果,如住院、IBD并发症、手术和死亡率似乎更好。同样,牛皮癣疾病活动相关的结果在GLP1RA队列中更好,但对其他IMIDs的影响受到文献稀少的限制。共有12项研究报告了代谢结果,包括体重减轻、血糖控制、腰围和脂质参数,均显示GLP1RAs的有益作用,这些结果与非ibd /IMID对照组相当。13项研究报告了不良事件(ae);胃肠道(GI) ae在GLP1RA组中较高(但大多数不严重)。结论:使用GLP1RA与IMIDs及伴随代谢紊乱患者更好的疾病活动性和代谢结局相关。注册:https://osf.io/jvmz6。
{"title":"Impact of GLP-1 analogues on immune-mediated inflammatory diseases: A systematic review","authors":"Chhagan L. Birda ,&nbsp;Fadwa Ibrahim ,&nbsp;Abhirup Chatterjee ,&nbsp;Anuraag Jena ,&nbsp;Vishal Sharma ,&nbsp;Shaji Sebastian","doi":"10.1016/j.autrev.2025.103936","DOIUrl":"10.1016/j.autrev.2025.103936","url":null,"abstract":"<div><h3>Objective</h3><div>Glucagon-like peptide-1 receptor agonists (GLP1RA) are believed to have anti-inflammatory properties apart from antidiabetic and anti-obesity effects.</div></div><div><h3>Methods</h3><div>We performed a systematic review to evaluate the efficacy and safety of GLP1RA in immune-mediated inflammatory disorders (IMIDs). A systematic search was done on 3rd April 2025 in PubMed, Scopus, and Embase for studies reporting the use of GLP1RA among patients with IMIDs. Because of significant heterogeneity and overlapping data originating from the same insurance databases, we decided against performing a data synthesis and meta-analysis. We summarised the data regarding clinical and metabolic outcomes in patients with IMIDs with/without the use of GLP1RA.</div></div><div><h3>Results</h3><div>Thirty-three studies (20 full text, 13 conference abstracts) were included, of which 20 studies focused on inflammatory bowel disease (IBD) and 13 on other IMIDs. Of the three studies reporting on new onset IBD/IMID in GLP1RA users, 2 showed a lower incidence. IBD therapy utilization was reported in 13 studies; steroid use was lower in 5 studies, but the data on the use of biologics were inconclusive. Other outcomes, like hospitalization, IBD complications, surgery, and mortality, seemed to be better in GLP1RA cohorts in a few of the studies. Similarly, psoriasis disease activity-related outcomes were better in the GLP1RA cohort, but the effect on other IMIDs was limited by sparse literature. A total of 12 studies reported metabolic outcomes, including weight loss, glycaemic control, waist circumference, and lipid parameters, all of which showed beneficial effects of GLP1RAs, and these results were comparable to non-IBD/IMID controls. Adverse events (AEs) were reported by 13 studies; gastrointestinal (GI) AEs were higher in the GLP1RA cohort (but the majority were non-severe).</div></div><div><h3>Conclusion</h3><div>GLP1RA use is associated with better disease activity and metabolic outcomes in patients with IMIDs and concomitant metabolic disorders.</div><div>Registration: <span><span>https://osf.io/jvmz6</span><svg><path></path></svg></span></div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103936"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278829","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
Sex-specific mechanisms in the pathogenesis and progression of chronic kidney disease 慢性肾脏疾病的发病和进展中的性别特异性机制。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103938
Guangtao Li , Zhiwei Xu , Hongxia Yang , Dan Zhang , Bin Liu , Yifan Song , Qianhui Li , Yanghe Zhang , Honglan Zhou , Yishu Wang
Chronic kidney disease (CKD) is a growing global public health concern, marked by increasing prevalence and substantial economic burden. Notably, CKD demonstrates significant physiological sex differences. Epidemiological evidence indicates that men are more susceptible to developing CKD in early to middle adulthood due to accelerated declines in renal function, whereas postmenopausal women exhibit a sharp rise in CKD incidence and progression. These findings suggest that sex hormones may play a critical regulatory role in CKD pathogenesis. The “bidirectional effects” of sex hormones are considered a fundamental mechanism driving these sex-based disparities. Androgens exacerbate renal inflammation and fibrosis by activating the TGF-β/TNF-α axis and the renin–angiotensin–aldosterone system (RAAS)/20-HETE pathway, in concert with NLRP3 inflammasome activation, thereby worsening glomerular hypertension and metabolic dysfunction. In contrast, estrogens exert protective effects by inhibiting RAAS activity, upregulating the ACE2/Ang-(1–7) pathway, activating the GPER/Sirt1 signaling network, and enhancing antioxidant capacity, thereby preserving renal hemodynamic homeostasis. Furthermore, this review incorporates a range of additional factors—including hormone-like compounds, sex-specific gut microbiota–host metabolic interactions, sex chromosome inactivation or loss, ectopic lipid deposition, and unfavorable lifestyle behaviors—to construct a comprehensive pathological model of sex-specific CKD progression. Elucidating the mechanisms by which sex differences influence kidney disease, and identifying sex-dependent contributors to CKD onset and advancement, may provide critical insights for developing personalized therapeutic strategies.
慢性肾脏疾病(CKD)是一个日益增长的全球公共卫生问题,其特点是患病率不断上升,经济负担沉重。值得注意的是,CKD表现出显著的生理性别差异。流行病学证据表明,由于肾功能加速下降,男性在成年早期至中期更容易发生CKD,而绝经后女性CKD发病率和进展急剧上升。这些发现提示性激素可能在CKD发病机制中起关键的调节作用。性激素的“双向效应”被认为是导致这些性别差异的根本机制。雄激素通过激活TGF-β/TNF-α轴和肾素-血管紧张素-醛固酮系统(RAAS)/20-HETE通路,协同NLRP3炎性体激活,加重肾小球高血压和代谢功能障碍,从而加重肾脏炎症和纤维化。相反,雌激素通过抑制RAAS活性、上调ACE2/Ang-(1-7)通路、激活GPER/Sirt1信号网络、增强抗氧化能力来发挥保护作用,从而维持肾脏血流动力学稳态。此外,本综述纳入了一系列其他因素,包括激素样化合物、性别特异性肠道微生物群-宿主代谢相互作用、性染色体失活或丢失、异位脂质沉积和不利的生活方式行为,以构建性别特异性CKD进展的综合病理模型。阐明性别差异影响肾脏疾病的机制,确定CKD发病和进展的性别依赖因素,可能为制定个性化治疗策略提供重要见解。
{"title":"Sex-specific mechanisms in the pathogenesis and progression of chronic kidney disease","authors":"Guangtao Li ,&nbsp;Zhiwei Xu ,&nbsp;Hongxia Yang ,&nbsp;Dan Zhang ,&nbsp;Bin Liu ,&nbsp;Yifan Song ,&nbsp;Qianhui Li ,&nbsp;Yanghe Zhang ,&nbsp;Honglan Zhou ,&nbsp;Yishu Wang","doi":"10.1016/j.autrev.2025.103938","DOIUrl":"10.1016/j.autrev.2025.103938","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is a growing global public health concern, marked by increasing prevalence and substantial economic burden. Notably, CKD demonstrates significant physiological sex differences. Epidemiological evidence indicates that men are more susceptible to developing CKD in early to middle adulthood due to accelerated declines in renal function, whereas postmenopausal women exhibit a sharp rise in CKD incidence and progression. These findings suggest that sex hormones may play a critical regulatory role in CKD pathogenesis. The “bidirectional effects” of sex hormones are considered a fundamental mechanism driving these sex-based disparities. Androgens exacerbate renal inflammation and fibrosis by activating the TGF-β/TNF-α axis and the renin–angiotensin–aldosterone system (RAAS)/20-HETE pathway, in concert with NLRP3 inflammasome activation, thereby worsening glomerular hypertension and metabolic dysfunction. In contrast, estrogens exert protective effects by inhibiting RAAS activity, upregulating the ACE2/Ang-(1–7) pathway, activating the GPER/Sirt1 signaling network, and enhancing antioxidant capacity, thereby preserving renal hemodynamic homeostasis. Furthermore, this review incorporates a range of additional factors—including hormone-like compounds, sex-specific gut microbiota–host metabolic interactions, sex chromosome inactivation or loss, ectopic lipid deposition, and unfavorable lifestyle behaviors—to construct a comprehensive pathological model of sex-specific CKD progression. Elucidating the mechanisms by which sex differences influence kidney disease, and identifying sex-dependent contributors to CKD onset and advancement, may provide critical insights for developing personalized therapeutic strategies.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103938"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312134","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
Are the 2023 ACR/EULAR classification criteria a step forward in the management of antiphospholipid syndrome? A literature-based and clinical practice appraisal 2023年ACR/EULAR分类标准是抗磷脂综合征管理的一个进步吗?基于文献和临床实践的评价。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103956
Jaume Alijotas-Reig , Joana Marques-Soares , Enrique Esteve-Valverde , Ariadna Anunciación-Llunell , Catalina Andrada , Monika Ockova , Ariella Hoxha , Munther A. Khamashta , Yehuda Shoenfeld , Francesc Miró-Mur
Antiphospholipid syndrome (APS) is an autoimmune disease (AID) without defined diagnostic criteria, but having classification criteria, as happens in most AID. Until 2023, we were using 2006 Sydney classification criteria. Although they had a research purposes, in the real life they have been used as a diagnostic tool, equating classification with diagnostic. From July 2023, these criteria were revisited by American College of Rheumatology and European League Against Rheumatism (ACR/EULAR) panel of experts. This recently reported set of classification criteria underlie that only should be used for research purposes. They prioritises specificity ̵ 99 % ̵ at the cost of sensitivity ̵ 84 % ̵ ACR/EULAR criteria consider 6 clinical and 2 laboratory domains. Although new clinical items have been included, improving overall the inclusion of patients and, indirectly diagnosis, i.e., thrombocytopenia, cardiac valvular involvement and microvascular thrombosis, a remarkable number of patients with putative aPL-related disorders could leave out of classification as having APS, and in the real life, losing the opportunity to manage them appropriately. Consequently, these patients will be prone to suffer new events, thrombotic or obstetric, as have been already demonstrated.
This manuscript focuses on the pros and cons of the clinical and laboratory domains of these new criteria and their impact not only on the clinical point of view, but also in the APS research field.
Using 6 clinical cases, we provide readers with a sense of diagnostic certainties and uncertainties, and their shortcomings in the context of the ACR/EULAR APS classification.
抗磷脂综合征(APS)是一种自身免疫性疾病(AID),没有明确的诊断标准,但有分类标准,正如大多数AID一样。直到2023年,我们使用的是2006年悉尼分类标准。虽然它们有研究目的,但在现实生活中,它们被用作诊断工具,将分类等同于诊断。从2023年7月起,美国风湿病学会和欧洲抗风湿病联盟(ACR/EULAR)专家小组重新审视了这些标准。最近报告的一套分类标准表明,只应用于研究目的。他们优先考虑特异性(99 %),以敏感性为代价(84 )ACR/EULAR标准考虑6个临床和2个实验室领域。虽然纳入了新的临床项目,总体上提高了患者的纳入和间接诊断,即血小板减少症、心瓣膜受累性和微血管血栓形成,但仍有相当数量的推定apl相关疾病患者可能被排除在APS的分类之外,在现实生活中失去了适当治疗的机会。因此,这些患者将容易遭受新的事件,血栓或产科,已经证明。这份手稿着重于这些新标准的临床和实验室领域的优点和缺点,以及它们不仅对临床观点的影响,而且对APS研究领域的影响。通过6个临床病例,我们为读者提供了诊断的确定性和不确定性,以及他们在ACR/EULAR APS分类背景下的缺点。
{"title":"Are the 2023 ACR/EULAR classification criteria a step forward in the management of antiphospholipid syndrome? A literature-based and clinical practice appraisal","authors":"Jaume Alijotas-Reig ,&nbsp;Joana Marques-Soares ,&nbsp;Enrique Esteve-Valverde ,&nbsp;Ariadna Anunciación-Llunell ,&nbsp;Catalina Andrada ,&nbsp;Monika Ockova ,&nbsp;Ariella Hoxha ,&nbsp;Munther A. Khamashta ,&nbsp;Yehuda Shoenfeld ,&nbsp;Francesc Miró-Mur","doi":"10.1016/j.autrev.2025.103956","DOIUrl":"10.1016/j.autrev.2025.103956","url":null,"abstract":"<div><div>Antiphospholipid syndrome (APS) is an autoimmune disease (AID) without defined diagnostic criteria, but having classification criteria, as happens in most AID. Until 2023, we were using 2006 Sydney classification criteria. Although they had a research purposes, in the real life they have been used as a diagnostic tool, equating classification with diagnostic. From July 2023, these criteria were revisited by American College of Rheumatology and European League Against Rheumatism (ACR/EULAR) panel of experts. This recently reported set of classification criteria underlie that only should be used for research purposes. They prioritises specificity ̵ 99 % ̵ at the cost of sensitivity ̵ 84 % ̵ ACR/EULAR criteria consider 6 clinical and 2 laboratory domains. Although new clinical items have been included, improving overall the inclusion of patients and, indirectly diagnosis, i.e., thrombocytopenia, cardiac valvular involvement and microvascular thrombosis, a remarkable number of patients with putative aPL-related disorders could leave out of classification as having APS, and in the real life, losing the opportunity to manage them appropriately. Consequently, these patients will be prone to suffer new events, thrombotic or obstetric, as have been already demonstrated.</div><div>This manuscript focuses on the pros and cons of the clinical and laboratory domains of these new criteria and their impact not only on the clinical point of view, but also in the APS research field.</div><div>Using 6 clinical cases, we provide readers with a sense of diagnostic certainties and uncertainties, and their shortcomings in the context of the ACR/EULAR APS classification.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103956"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145421149","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
MTHFR polymorphisms in autoimmune diseases: Mechanistic and clinical perspectives 自身免疫性疾病中的MTHFR多态性:机制和临床观点。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103939
Ting Sun , Yuxian Wu , Lingyun Kong , Jingtong Wang , Feng Zhang , Yang Liu , Jie Gao , Yaoyang Liu
The methylenetetrahydrofolate reductase (MTHFR) gene encodes a crucial enzyme in folate metabolism, serving as a central regulator of homocysteine homeostasis and one‑carbon metabolic pathways. This review synthesizes current evidence on the mechanistic and clinical implications of two common MTHFR polymorphisms, C677T and A1298C, in autoimmune pathogenesis. We critically examine their contributions to inflammatory responses, endothelial dysfunction, immune imbalance, and epigenetic modifications. Furthermore, we analyze population-specific associations between these variants and susceptibility to eight autoimmune disorders, genotype-phenotype correlations related to clinical manifestations and comorbidities, as well as pharmacogenomic interactions influencing response to methotrexate therapy. By integrating genetic, molecular, and clinical insights, this review highlights the translational potential of MTHFR genotyping for improving risk stratification and personalized treatment strategies in autoimmune and immune-mediated inflammatory conditions.
亚甲基四氢叶酸还原酶(MTHFR)基因编码叶酸代谢中的一种关键酶,作为同型半胱氨酸稳态和单碳代谢途径的中心调节因子。本文综述了目前关于两种常见MTHFR多态性C677T和A1298C在自身免疫发病机制中的机制和临床意义的证据。我们严格检查他们的贡献炎症反应,内皮功能障碍,免疫失衡和表观遗传修饰。此外,我们分析了这些变异与8种自身免疫性疾病易感性之间的人群特异性关联,与临床表现和合并症相关的基因型-表型相关性,以及影响对甲氨蝶呤治疗反应的药物基因组学相互作用。通过整合遗传、分子和临床见解,本综述强调了MTHFR基因分型在改善自身免疫性和免疫介导性炎症的风险分层和个性化治疗策略方面的转化潜力。
{"title":"MTHFR polymorphisms in autoimmune diseases: Mechanistic and clinical perspectives","authors":"Ting Sun ,&nbsp;Yuxian Wu ,&nbsp;Lingyun Kong ,&nbsp;Jingtong Wang ,&nbsp;Feng Zhang ,&nbsp;Yang Liu ,&nbsp;Jie Gao ,&nbsp;Yaoyang Liu","doi":"10.1016/j.autrev.2025.103939","DOIUrl":"10.1016/j.autrev.2025.103939","url":null,"abstract":"<div><div>The methylenetetrahydrofolate reductase (<em>MTHFR</em>) gene encodes a crucial enzyme in folate metabolism, serving as a central regulator of homocysteine homeostasis and one‑carbon metabolic pathways. This review synthesizes current evidence on the mechanistic and clinical implications of two common <em>MTHFR</em> polymorphisms, C677T and A1298C, in autoimmune pathogenesis. We critically examine their contributions to inflammatory responses, endothelial dysfunction, immune imbalance, and epigenetic modifications. Furthermore, we analyze population-specific associations between these variants and susceptibility to eight autoimmune disorders, genotype-phenotype correlations related to clinical manifestations and comorbidities, as well as pharmacogenomic interactions influencing response to methotrexate therapy. By integrating genetic, molecular, and clinical insights, this review highlights the translational potential of <em>MTHFR</em> genotyping for improving risk stratification and personalized treatment strategies in autoimmune and immune-mediated inflammatory conditions.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103939"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285537","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
Immune checkpoint inhibitor-induced inflammatory arthritis vs rheumatoid arthritis: A comparative review 免疫检查点抑制剂诱导的炎性关节炎与类风湿关节炎:比较回顾。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103943
Iliopoulos Georgios , Sideridou Fani , Bogdanos Dmitrios , Liew David , Daoussis Dimitrios
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are frequently accompanied by immune-related adverse events (irAEs). Among these, ICI-induced inflammatory arthritis (ICI-IA) has emerged as the most common musculoskeletal toxicity, often mimicking rheumatoid arthritis (RA) in its clinical and imaging features. This narrative review synthesizes current evidence comparing ICI-IA with RA across epidemiology, pathophysiology, clinical presentation, imaging, treatment, and prognosis. While both entities share overlapping manifestations such as polyarthritis, synovitis, and joint erosions, ICI-IA is typically seronegative, arises subacutely after ICI initiation, and exhibits distinct immunopathologic signatures, including cytotoxic CD8+ T-cell predominance and unique B-cell alterations. ICI-IA may persist after ICI cessation, with chronic disease linked to improved oncologic outcomes. Therapeutic strategies require balancing arthritis control and preservation of anti-tumor immunity. Glucocorticoids and conventional disease modifying anti-rheumatic drugs (cDMARDs) are key players with proven safety and efficacy, whereas biologic therapies remain reserved for severe or refractory cases mainly due to cancer progression concerns. Furthermore, early rheumatology referral improves patient outcomes and reduces glucocorticoid exposure. Understanding the differences between ICI-IA and RA is essential for optimizing diagnosis, guiding individualized approach and applying precision medicine at the crossroads of oncology and rheumatology.
免疫检查点抑制剂(ICIs)已经改变了肿瘤的治疗前景,但经常伴随着免疫相关不良事件(irAEs)。其中,ici诱导的炎症性关节炎(ICI-IA)已成为最常见的肌肉骨骼毒性,其临床和影像学特征通常与类风湿关节炎(RA)相似。本文综述了ICI-IA与RA在流行病学、病理生理学、临床表现、影像学、治疗和预后方面的比较证据。虽然这两种疾病有重叠的表现,如多关节炎、滑膜炎和关节糜坏,但ICI- ia通常是血清阴性的,在ICI开始后亚急性出现,并表现出独特的免疫病理特征,包括细胞毒性CD8+ t细胞优势和独特的b细胞改变。ICI- ia可能在ICI停止后持续存在,慢性疾病与肿瘤预后改善有关。治疗策略需要平衡关节炎控制和保持抗肿瘤免疫。糖皮质激素和常规疾病修饰抗风湿药物(cDMARDs)是安全性和有效性被证明的关键因素,而生物疗法仍然保留用于严重或难治性病例,主要是由于癌症进展的担忧。此外,早期风湿病转诊可改善患者预后并减少糖皮质激素暴露。了解ICI-IA和RA之间的差异对于优化诊断、指导个体化治疗以及在肿瘤学和风湿病学交叉领域应用精准医学至关重要。
{"title":"Immune checkpoint inhibitor-induced inflammatory arthritis vs rheumatoid arthritis: A comparative review","authors":"Iliopoulos Georgios ,&nbsp;Sideridou Fani ,&nbsp;Bogdanos Dmitrios ,&nbsp;Liew David ,&nbsp;Daoussis Dimitrios","doi":"10.1016/j.autrev.2025.103943","DOIUrl":"10.1016/j.autrev.2025.103943","url":null,"abstract":"<div><div>Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are frequently accompanied by immune-related adverse events (irAEs). Among these, ICI-induced inflammatory arthritis (ICI-IA) has emerged as the most common musculoskeletal toxicity, often mimicking rheumatoid arthritis (RA) in its clinical and imaging features. This narrative review synthesizes current evidence comparing ICI-IA with RA across epidemiology, pathophysiology, clinical presentation, imaging, treatment, and prognosis. While both entities share overlapping manifestations such as polyarthritis, synovitis, and joint erosions, ICI-IA is typically seronegative, arises subacutely after ICI initiation, and exhibits distinct immunopathologic signatures, including cytotoxic CD8+ T-cell predominance and unique B-cell alterations. ICI-IA may persist after ICI cessation, with chronic disease linked to improved oncologic outcomes. Therapeutic strategies require balancing arthritis control and preservation of anti-tumor immunity. Glucocorticoids and conventional disease modifying anti-rheumatic drugs (cDMARDs) are key players with proven safety and efficacy, whereas biologic therapies remain reserved for severe or refractory cases mainly due to cancer progression concerns. Furthermore, early rheumatology referral improves patient outcomes and reduces glucocorticoid exposure. Understanding the differences between ICI-IA and RA is essential for optimizing diagnosis, guiding individualized approach and applying precision medicine at the crossroads of oncology and rheumatology.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103943"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336269","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
VE/VCO2 at ventilatory threshold and peak VO2 in CPET studies of patients with scleroderma-associated PAH: A systematic review and meta-analyses 硬皮病相关PAH患者的CPET研究中通气阈值的VE/VCO2和峰值VO2:系统回顾和荟萃分析
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103942
Julie Better , Sylvie Leroy , Maarten K. Ninaber , Georgia Trakada , Bilge Kesikburun , Stephan Rosenkranz , Ralph Ewert , Dirk Habedank , Daniel Dumitrescu , Yanis Kouchit , Nihal Martis

Context

Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in patients with systemic sclerosis (SSc). Cardiopulmonary exercise testing (CPET) has been studied to detect SSc-associated PAH.

Objectives

To evaluate the diagnostic value of the ventilatory equivalent for CO2 at anaerobic or ventilatory threshold [VE/VCO2(VeT)] and peak oxygen uptake (peak VO2) for SSc-associated PAH obtained by CPET.

Methods

A systematic database search from 1993 to 2024 and meta-analyses were performed according to PRISMA guidelines to include original studies relating to SSc and CPET reporting VE/VCO2(VeT) and peak VO2. The random-effects model was chosen for the meta-analyses studying VE/VCO2(VeT), indexed and predicted percentage (%pred.) peak VO2, respectively. Meta-regression was only performed for VE/VCO2(VeT) with covariates defined as the percentage of limited cutaneous disease, percentage of interstitial lung disease, and %pred. of peak VO2.

Results

Out of 206 studies, 941 SSc patients from 15 studies were included. VE/VCO2(VeT) (11 studies, n = 850) was statistically lower in patients without PAH (32.68 ± 5.42 vs. 39.81 ± 9.32) with a mean effect size of −1.182 (95 %CI, −1.691 to −0.672; p < 0.001) (I2 = 86 %). The mean effect size for weight-indexed peak VO2 (11 studies, n = 848) was 0.713 (95 %CI, 0.371 to 1.054; p < 0.001) with higher values in patients without PAH (16.47 ± 4.62 vs. 13.61 ± 4.16 mL/kg/mn) (I2 = 70 %). Similarly, the mean effect size for %pred. Peak VO2 (12 studies, n = 850) was 0.659 (95 %CI, 0.425 to 0.894; p < 0.001) reflecting higher values in patients without PAH (74.00 ± 17.50 vs. 54.84 ± 18.14 %pred.) (I2 = 37 %). Meta-regression analysis of data from 7 studies did not yield significant p values for the covariates.

Conclusions

The effect size of each meta-analysis indicates that higher VE/VCO2(VeT) and lower peak VO2 may be considered as independent CPET markers of PAH in patients with SSc. CPET is a non-invasive and safe procedure for exploring dyspnoea in patients with SSc and, in association with conventional imaging techniques, may provide a reliable assessment of the presence of PAH.
背景:肺动脉高压(PAH)是系统性硬化症(SSc)患者死亡的主要原因之一。心肺运动试验(CPET)已被研究用于检测ssc相关的PAH。目的:评价CPET获得的无氧或通气阈值CO2通气当量[VE/VCO2(VeT)]和摄氧量峰值(VO2峰值)对ssc相关性PAH的诊断价值。方法:对1993 - 2024年的数据库进行系统检索,并根据PRISMA指南进行meta分析,纳入与SSc和CPET报告的VE/VCO2(VeT)和峰值VO2相关的原始研究。随机效应模型分别用于研究VE/VCO2(VeT)、指数和预测百分比(%pred.)峰值VO2的meta分析。仅对VE/VCO2(VeT)进行meta回归,协变量定义为局限性皮肤病百分比、间质性肺疾病百分比和pred %。VO2的峰值。结果:在206项研究中,纳入了来自15项研究的941例SSc患者。VE / VCO2(兽医)(11个研究中,n = 850)在统计学上低的病人没有多环芳烃(32.68 ±  5.42和39.81±9.32 )平均效应值为-1.182(95 % CI, -1.691 - -0.672; p 2 = 86 %)。体重指数峰值VO2的平均效应大小(11项研究,n = 848)为0.713(95 %CI, 0.371 ~ 1.054; p 2 = 70 %)。同样,%pred的平均效应大小。峰值VO2(12项研究,n = 850)为0.659(95 %CI, 0.425 ~ 0.894; p 2 = 37 %)。对7项研究的数据进行meta回归分析,协变量的p值均不显著。结论:各荟萃分析的效应大小表明,较高的VE/VCO2(VeT)和较低的峰值VO2可被视为SSc患者PAH的独立CPET标志物。CPET是一种无创、安全的检查SSc患者呼吸困难的方法,与常规成像技术相结合,可以可靠地评估PAH的存在。
{"title":"VE/VCO2 at ventilatory threshold and peak VO2 in CPET studies of patients with scleroderma-associated PAH: A systematic review and meta-analyses","authors":"Julie Better ,&nbsp;Sylvie Leroy ,&nbsp;Maarten K. Ninaber ,&nbsp;Georgia Trakada ,&nbsp;Bilge Kesikburun ,&nbsp;Stephan Rosenkranz ,&nbsp;Ralph Ewert ,&nbsp;Dirk Habedank ,&nbsp;Daniel Dumitrescu ,&nbsp;Yanis Kouchit ,&nbsp;Nihal Martis","doi":"10.1016/j.autrev.2025.103942","DOIUrl":"10.1016/j.autrev.2025.103942","url":null,"abstract":"<div><h3>Context</h3><div>Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in patients with systemic sclerosis (SSc). Cardiopulmonary exercise testing (CPET) has been studied to detect SSc-associated PAH.</div></div><div><h3>Objectives</h3><div>To evaluate the diagnostic value of the ventilatory equivalent for CO<sub>2</sub> at anaerobic or ventilatory threshold [VE/VCO<sub>2</sub>(VeT)] and peak oxygen uptake (peak VO<sub>2</sub>) for SSc-associated PAH obtained by CPET.</div></div><div><h3>Methods</h3><div>A systematic database search from 1993 to 2024 and meta-analyses were performed according to PRISMA guidelines to include original studies relating to SSc and CPET reporting VE/VCO<sub>2</sub>(VeT) and peak VO<sub>2</sub>. The random-effects model was chosen for the meta-analyses studying VE/VCO<sub>2</sub>(VeT), indexed and predicted percentage (%pred.) peak VO<sub>2</sub>, respectively. Meta-regression was only performed for VE/VCO<sub>2</sub>(VeT) with covariates defined as the percentage of limited cutaneous disease, percentage of interstitial lung disease, and %pred. of peak VO<sub>2</sub>.</div></div><div><h3>Results</h3><div>Out of 206 studies, 941 SSc patients from 15 studies were included. VE/VCO<sub>2</sub>(VeT) (11 studies, <em>n</em> = 850) was statistically lower in patients without PAH (32.68 ± 5.42 vs. 39.81 ± 9.32) with a mean effect size of −1.182 (95 %CI, −1.691 to −0.672; <em>p</em> &lt; 0.001) (I<sup>2</sup> = 86 %). The mean effect size for weight-indexed peak VO<sub>2</sub> (11 studies, <em>n</em> = 848) was 0.713 (95 %CI, 0.371 to 1.054; <em>p</em> &lt; 0.001) with higher values in patients without PAH (16.47 ± 4.62 vs. 13.61 ± 4.16 mL/kg/mn) (I<sup>2</sup> = 70 %). Similarly, the mean effect size for %pred. Peak VO<sub>2</sub> (12 studies, <em>n</em> = 850) was 0.659 (95 %CI, 0.425 to 0.894; p &lt; 0.001) reflecting higher values in patients without PAH (74.00 ± 17.50 vs. 54.84 ± 18.14 %pred.) (I<sup>2</sup> = 37 %). Meta-regression analysis of data from 7 studies did not yield significant <em>p</em> values for the covariates.</div></div><div><h3>Conclusions</h3><div>The effect size of each meta-analysis indicates that higher VE/VCO<sub>2</sub>(VeT) and lower peak VO<sub>2</sub> may be considered as independent CPET markers of PAH in patients with SSc. CPET is a non-invasive and safe procedure for exploring dyspnoea in patients with SSc and, in association with conventional imaging techniques, may provide a reliable assessment of the presence of PAH.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103942"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353381","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
Environmental toxins and toxic metals in autoimmune diseases: Sex differences, hormonal influences, and immune dysregulation 自身免疫性疾病中的环境毒素和有毒金属:性别差异、激素影响和免疫失调。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.autrev.2025.103955
Geir Bjørklund , David R. Wallace , Kimiya Kangarlou , Fahimida Hossain , Massimiliano Peana
Environmental toxins, including toxic metal(oid)s such as mercury, lead, cadmium, and arsenic, as well as endocrine-disrupting chemicals like bisphenol A and phthalates, play a critical role in the onset and progression of autoimmune diseases. These substances accumulate in biological tissues and disrupt immune homeostasis through oxidative stress, molecular mimicry, and epigenetic modifications, mechanisms that contribute to autoantibody production and chronic inflammation, hallmarks of autoimmunity. Women are disproportionately affected by autoimmune diseases due to inherent differences in immune function, hormonal regulation, and genetic susceptibility. Estrogen, a key immunomodulatory hormone, can amplify immune responses and promote autoantibody generation. Its interaction with environmental toxins further exacerbates immune dysregulation, increasing female vulnerability to conditions such as systemic lupus erythematosus, rheumatoid arthritis, and autoimmune thyroid disorders. Hormonal fluctuations during puberty, pregnancy, and menopause additionally influence toxin metabolism and detoxification efficiency, compounding the risk of immune imbalance and disease onset in women. This review synthesizes current evidence on the mechanisms through which environmental toxicants contribute to autoimmune pathogenesis, with particular focus on sex-specific vulnerabilities. It explores the role of hormonal-immune-environment interactions across the female lifespan and highlights emerging research on epigenetic inheritance, gut dysbiosis, and biomarker development. By integrating mechanistic, epidemiological, and clinical findings, this review aims to inform targeted strategies for prevention, early detection, and risk reduction of environmentally driven autoimmune diseases.
环境毒素,包括有毒金属(类),如汞、铅、镉和砷,以及内分泌干扰化学物质,如双酚A和邻苯二甲酸盐,在自身免疫性疾病的发生和发展中起着关键作用。这些物质在生物组织中积累,通过氧化应激、分子模仿和表观遗传修饰破坏免疫稳态,这些机制有助于自身抗体的产生和慢性炎症,这是自身免疫的标志。由于免疫功能、激素调节和遗传易感性的固有差异,妇女受到自身免疫性疾病的影响不成比例。雌激素是一种重要的免疫调节激素,可以增强免疫反应,促进自身抗体的产生。它与环境毒素的相互作用进一步加剧了免疫失调,增加了女性对系统性红斑狼疮、类风湿性关节炎和自身免疫性甲状腺疾病等疾病的易感性。青春期、孕期和更年期的荷尔蒙波动还会影响毒素代谢和解毒效率,增加女性免疫失衡和发病的风险。这篇综述综合了目前关于环境毒物促进自身免疫发病机制的证据,特别关注性别特异性脆弱性。它探讨了激素-免疫-环境相互作用在女性生命周期中的作用,并重点介绍了表观遗传、肠道生态失调和生物标志物发育方面的新兴研究。通过整合机制、流行病学和临床研究结果,本综述旨在为环境驱动型自身免疫性疾病的预防、早期发现和降低风险提供有针对性的策略。
{"title":"Environmental toxins and toxic metals in autoimmune diseases: Sex differences, hormonal influences, and immune dysregulation","authors":"Geir Bjørklund ,&nbsp;David R. Wallace ,&nbsp;Kimiya Kangarlou ,&nbsp;Fahimida Hossain ,&nbsp;Massimiliano Peana","doi":"10.1016/j.autrev.2025.103955","DOIUrl":"10.1016/j.autrev.2025.103955","url":null,"abstract":"<div><div>Environmental toxins, including toxic metal(<em>oid</em>)s such as mercury, lead, cadmium, and arsenic, as well as endocrine-disrupting chemicals like bisphenol A and phthalates, play a critical role in the onset and progression of autoimmune diseases. These substances accumulate in biological tissues and disrupt immune homeostasis through oxidative stress, molecular mimicry, and epigenetic modifications, mechanisms that contribute to autoantibody production and chronic inflammation, hallmarks of autoimmunity. Women are disproportionately affected by autoimmune diseases due to inherent differences in immune function, hormonal regulation, and genetic susceptibility. Estrogen, a key immunomodulatory hormone, can amplify immune responses and promote autoantibody generation. Its interaction with environmental toxins further exacerbates immune dysregulation, increasing female vulnerability to conditions such as systemic lupus erythematosus, rheumatoid arthritis, and autoimmune thyroid disorders. Hormonal fluctuations during puberty, pregnancy, and menopause additionally influence toxin metabolism and detoxification efficiency, compounding the risk of immune imbalance and disease onset in women. This review synthesizes current evidence on the mechanisms through which environmental toxicants contribute to autoimmune pathogenesis, with particular focus on sex-specific vulnerabilities. It explores the role of hormonal-immune-environment interactions across the female lifespan and highlights emerging research on epigenetic inheritance, gut dysbiosis, and biomarker development. By integrating mechanistic, epidemiological, and clinical findings, this review aims to inform targeted strategies for prevention, early detection, and risk reduction of environmentally driven autoimmune diseases.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103955"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145421205","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
The Trm-Treg Axis as a tissue-encoded immune checkpoint in chronic inflammation and autoimmunity Trm-Treg轴在慢性炎症和自身免疫中的组织编码免疫检查点作用
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-12-24 DOI: 10.1016/j.autrev.2025.103977
Liang Li , Yumin Xia , Yale Liu
Tissue-resident memory T (Trm) cells, once heralded as gatekeepers of localized immune protection, have emerged as central players in the pathogenesis of chronic inflammation and autoimmunity at epithelial barriers. At the heart of this immunological paradox lies the dynamic interplay between Trm and regulatory T (Treg) cells—a tissue-encoded checkpoint that calibrates immune defense against the need for tolerance and repair. Disruption of this axis unleashes the latent pathogenicity of Trm cells, fueling persistent inflammation, epithelial dysfunction, and disease relapse. Here, we propose that the Trm-Treg interaction acts as a molecular rheostat that tunes immune homeostasis at barrier sites. We dissect the tissue-specific mechanisms that sustain this alliance, highlight its failure in diseases such as inflammatory bowel disease (IBD), psoriasis, and chronic obstructive pulmonary disease (COPD), and explore emerging therapeutic strategies aimed at recalibrating this immune checkpoint to restore durable epithelial tolerance.
组织常驻记忆T (Trm)细胞,曾经被认为是局部免疫保护的守门人,已经成为慢性炎症和上皮屏障自身免疫发病机制的核心参与者。这一免疫学悖论的核心在于Trm和调节性T细胞(Treg)之间的动态相互作用。Treg是一种组织编码的检查点,校准免疫防御对耐受和修复的需求。这条轴的破坏释放了Trm细胞的潜伏致病性,助长了持续的炎症、上皮功能障碍和疾病复发。在这里,我们提出Trm-Treg相互作用作为一种分子变阻器,调节屏障部位的免疫稳态。我们剖析了维持这种联盟的组织特异性机制,强调了其在炎症性肠病(IBD)、牛皮癣和慢性阻塞性肺疾病(COPD)等疾病中的失败,并探索了旨在重新校准这种免疫检查点以恢复持久上皮耐受的新兴治疗策略。
{"title":"The Trm-Treg Axis as a tissue-encoded immune checkpoint in chronic inflammation and autoimmunity","authors":"Liang Li ,&nbsp;Yumin Xia ,&nbsp;Yale Liu","doi":"10.1016/j.autrev.2025.103977","DOIUrl":"10.1016/j.autrev.2025.103977","url":null,"abstract":"<div><div>Tissue-resident memory T (Trm) cells, once heralded as gatekeepers of localized immune protection, have emerged as central players in the pathogenesis of chronic inflammation and autoimmunity at epithelial barriers. At the heart of this immunological paradox lies the dynamic interplay between Trm and regulatory T (Treg) cells—a tissue-encoded checkpoint that calibrates immune defense against the need for tolerance and repair. Disruption of this axis unleashes the latent pathogenicity of Trm cells, fueling persistent inflammation, epithelial dysfunction, and disease relapse. Here, we propose that the Trm-Treg interaction acts as a molecular rheostat that tunes immune homeostasis at barrier sites. We dissect the tissue-specific mechanisms that sustain this alliance, highlight its failure in diseases such as inflammatory bowel disease (IBD), psoriasis, and chronic obstructive pulmonary disease (COPD), and explore emerging therapeutic strategies aimed at recalibrating this immune checkpoint to restore durable epithelial tolerance.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103977"},"PeriodicalIF":8.3,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839645","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
The role of sleep in multiple sclerosis. 睡眠在多发性硬化症中的作用。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-28 Epub Date: 2025-08-06 DOI: 10.1016/j.autrev.2025.103902
Susanna Cordone, Valentina Alfonsi, Luigi De Gennaro

Multiple Sclerosis (MS) is an autoimmunity-related disorder that mainly affects young adults. The high prevalence of the disease and its impact on patients' quality of life led researchers to investigate the etiopathogenesis of the disease to identify possible modifiable factors and consequent effective intervention strategies. Recent hypotheses suggest that the etiopathogenesis of MS is multifactorial and includes factors related to the immune system, neuroinflammation and neurodegeneration. In this scenario, sleep seems to have a close indirect relationship with MS, through its relationship with each of those factors and given the high incidence of sleep disorders in the MS population. Furthermore, given the growing interest of research in the mechanisms underlying MS and therapies able to alleviate MS-related symptoms at all stages of the disease, a more in-depth study of the role of sleep and its loss and disturbances and the factors intrinsically related to sleep and MS could be useful both to investigate the etiopathogenetic factors of MS and to develop non-invasive intervention strategies for MS treatment.

多发性硬化症(MS)是一种主要影响年轻人的自身免疫相关疾病。该疾病的高患病率及其对患者生活质量的影响促使研究人员调查该疾病的发病机制,以确定可能的可改变因素和随之而来的有效干预策略。最近的假设认为MS的发病是多因素的,包括与免疫系统、神经炎症和神经变性有关的因素。在这种情况下,睡眠似乎与多发性硬化症有密切的间接关系,通过它与这些因素的关系,并考虑到多发性硬化症人群中睡眠障碍的高发病率。此外,鉴于人们对多发性硬化症的发病机制和治疗方法的研究兴趣日益浓厚,对睡眠的作用、睡眠的丧失和障碍以及与睡眠和多发性硬化症内在相关的因素进行更深入的研究,可能有助于研究多发性硬化症的发病因素,并为多发性硬化症的治疗制定非侵入性干预策略。
{"title":"The role of sleep in multiple sclerosis.","authors":"Susanna Cordone, Valentina Alfonsi, Luigi De Gennaro","doi":"10.1016/j.autrev.2025.103902","DOIUrl":"10.1016/j.autrev.2025.103902","url":null,"abstract":"<p><p>Multiple Sclerosis (MS) is an autoimmunity-related disorder that mainly affects young adults. The high prevalence of the disease and its impact on patients' quality of life led researchers to investigate the etiopathogenesis of the disease to identify possible modifiable factors and consequent effective intervention strategies. Recent hypotheses suggest that the etiopathogenesis of MS is multifactorial and includes factors related to the immune system, neuroinflammation and neurodegeneration. In this scenario, sleep seems to have a close indirect relationship with MS, through its relationship with each of those factors and given the high incidence of sleep disorders in the MS population. Furthermore, given the growing interest of research in the mechanisms underlying MS and therapies able to alleviate MS-related symptoms at all stages of the disease, a more in-depth study of the role of sleep and its loss and disturbances and the factors intrinsically related to sleep and MS could be useful both to investigate the etiopathogenetic factors of MS and to develop non-invasive intervention strategies for MS treatment.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"103902"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798049","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
Adjusting fragility metrics for unequal trial randomizations 调整不平等试验随机化的脆弱性指标。
IF 8.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-09-17 DOI: 10.1016/j.autrev.2025.103935
Thomas F. Heston
{"title":"Adjusting fragility metrics for unequal trial randomizations","authors":"Thomas F. Heston","doi":"10.1016/j.autrev.2025.103935","DOIUrl":"10.1016/j.autrev.2025.103935","url":null,"abstract":"","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103935"},"PeriodicalIF":8.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091119","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
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1