Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103958
Siying Deng, Ziwei Hu, Shaozhe Cai, Lingli Dong
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological auto-antibody production and severe immune dysregulation. Dysfunction in regulated cell death (RCD) pathways is crucial in SLE development. Abnormal cell death and cell debris clearance disorder within tissues promote the exposure and accumulation of auto-antigens, activate self-reaction B cells, and amplify interferon type I (IFN-I) reaction. Meanwhile, immune microenvironment disorder caused by abnormal RCD of immune cells exacerbate this response. The review systematically expounds the pathogenic mechanisms of both classical and novel RCD pathways in SLE. By comparing shared and disease-specific RCD dysregulation between SLE and other autoimmune diseases, we evaluate innovative RCD-targeted therapies, offering new insights on SLE pathogenesis and precision treatment.
{"title":"Regulated cell death in systemic lupus erythematosus: Key pathways and targeted therapies","authors":"Siying Deng, Ziwei Hu, Shaozhe Cai, Lingli Dong","doi":"10.1016/j.autrev.2025.103958","DOIUrl":"10.1016/j.autrev.2025.103958","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological auto-antibody production and severe immune dysregulation. Dysfunction in regulated cell death (RCD) pathways is crucial in SLE development. Abnormal cell death and cell debris clearance disorder within tissues promote the exposure and accumulation of auto-antigens, activate self-reaction B cells, and amplify interferon type I (IFN-I) reaction. Meanwhile, immune microenvironment disorder caused by abnormal RCD of immune cells exacerbate this response. The review systematically expounds the pathogenic mechanisms of both classical and novel RCD pathways in SLE. By comparing shared and disease-specific RCD dysregulation between SLE and other autoimmune diseases, we evaluate innovative RCD-targeted therapies, offering new insights on SLE pathogenesis and precision treatment.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103958"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562454","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103941
Chao Hu , Jingyi Wu , Yuanyuan Luo , Yichun Zhu, Runyu Chang, Suhai Qian, Xinghong Ding
Objectives
Weather conditions have been suggested to influence the clinical manifestations of rheumatoid arthritis (RA), but current evidence remains inconsistent. This meta-analysis aimed to evaluate the association between meteorological factors and RA disease activity.
Methods
PubMed, Web of Science, EMBASE, and the Cochrane Library were searched from inception to March 25, 2025. Two reviewers independently screened and extracted data according to predefined criteria. A random-effects model was used to pool results. Meta-regression analyses were performed to explore potential sources of heterogeneity across studies. Publication bias was assessed using Egger's test, Begg's test, and funnel plots. Sensitivity analyses were conducted using a leave-one-out approach to examine the impact of each individual study on the pooled estimates.
Results
A total of 16,503 records were identified through the literature search, of which eight studies met the inclusion criteria and were included in the meta-analysis. The pooled results indicated no significant overall association between temperature, atmospheric pressure, humidity, or wind speed and RA pain. In addition, temperature was negatively correlated with TJC (pooled Fisher's Z = −0.08, 95 % CI −0.151 to −0.009, P = 0.028 < 0.05, summary r = −0.080, 95 % CI −0.150 to −0.009), and atmospheric pressure was negatively correlated with SJC (pooled Fisher's Z = −0.075, 95 % CI −0.115 to −0.036, P < 0.001, summary r = −0.075, 95 % CI −0.114 to −0.036), both with low heterogeneity. No other significant associations were observed.
Conclusions
Specific meteorological factors, temperature and atmospheric pressure, may modestly affect RA symptoms. These findings may contribute to individualized disease management and guide future research on environmental influences in autoimmune diseases.
目的：天气条件已被认为会影响类风湿关节炎（RA）的临床表现，但目前的证据仍不一致。本荟萃分析旨在评估气象因素与类风湿性关节炎疾病活动之间的关系。方法：检索PubMed、Web of Science、EMBASE和Cochrane Library自成立至2025年3月25日的文献。两名审稿人根据预定义的标准独立筛选和提取数据。随机效应模型用于汇总结果。进行meta回归分析以探索研究间异质性的潜在来源。采用Egger检验、Begg检验和漏斗图评估发表偏倚。敏感度分析采用留一方法进行，以检查每个单独研究对汇总估计的影响。结果：通过文献检索共检索到16503条记录，其中8项研究符合纳入标准，被纳入meta分析。综合结果表明，温度、大气压、湿度或风速与类风湿性关节炎疼痛之间没有显著的总体关联。此外，温度与TJC呈负相关（合并Fisher’s Z = -0.08,95 % CI -0.151 ~ -0.009, P = 0.028 ）结论：特定的气象因素，温度和大气压力可能对RA症状有轻微影响。这些发现可能有助于个体化疾病管理，并指导未来对自身免疫性疾病环境影响的研究。
{"title":"Association between weather conditions and rheumatoid arthritis: A systematic review and meta-analysis","authors":"Chao Hu , Jingyi Wu , Yuanyuan Luo , Yichun Zhu, Runyu Chang, Suhai Qian, Xinghong Ding","doi":"10.1016/j.autrev.2025.103941","DOIUrl":"10.1016/j.autrev.2025.103941","url":null,"abstract":"<div><h3>Objectives</h3><div>Weather conditions have been suggested to influence the clinical manifestations of rheumatoid arthritis (RA), but current evidence remains inconsistent. This meta-analysis aimed to evaluate the association between meteorological factors and RA disease activity.</div></div><div><h3>Methods</h3><div>PubMed, Web of Science, EMBASE, and the Cochrane Library were searched from inception to March 25, 2025. Two reviewers independently screened and extracted data according to predefined criteria. A random-effects model was used to pool results. Meta-regression analyses were performed to explore potential sources of heterogeneity across studies. Publication bias was assessed using Egger's test, Begg's test, and funnel plots. Sensitivity analyses were conducted using a leave-one-out approach to examine the impact of each individual study on the pooled estimates.</div></div><div><h3>Results</h3><div>A total of 16,503 records were identified through the literature search, of which eight studies met the inclusion criteria and were included in the meta-analysis. The pooled results indicated no significant overall association between temperature, atmospheric pressure, humidity, or wind speed and RA pain. In addition, temperature was negatively correlated with TJC (pooled Fisher's Z = −0.08, 95 % CI −0.151 to −0.009, <em>P</em> = 0.028 < 0.05, summary <em>r</em> = −0.080, 95 % CI −0.150 to −0.009), and atmospheric pressure was negatively correlated with SJC (pooled Fisher's Z = −0.075, 95 % CI −0.115 to −0.036, <em>P</em> < 0.001, summary <em>r</em> = −0.075, 95 % CI −0.114 to −0.036), both with low heterogeneity. No other significant associations were observed.</div></div><div><h3>Conclusions</h3><div>Specific meteorological factors, temperature and atmospheric pressure, may modestly affect RA symptoms. These findings may contribute to individualized disease management and guide future research on environmental influences in autoimmune diseases.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103941"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285536","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103924
Jan Willem Cohen Tervaert
Many different drugs and/or vaccines may cause vasculitis which can be sometimes very severe.
The clinical presentation varies from isolated skin vasculitis to multi-organ involvement with pulmonary-renal manifestations and/or cerebral vasculitis.
Whereas causality is difficult to prove and rechallenges are considered unethical, pathophysiological mechanisms suggesting causality have been demonstrated for drugs such as hydralazine, propylthiouracil, levamisole, and immune checkpoint inhibitors.
An important pathophysiological mechanism of drug-induced anti-neutrophil autoantibody (ANCA)-associated vasculitis is the fact that several drugs have been demonstrated to increase the formation of neutrophil extracellular traps which may result in the development of autoimmunity.
The first step in medical management of drug-induced ANCA-associated vasculitis is discontinuation of the offending drug and a transparent discussion with the patient regarding the possibility that the drug or the vaccine may have caused vasculitis. Additional treatment with steroids and immunosuppressants is often needed in more severe cases of ANCA-associated vasculitis. In general, however, the long-term prognosis of drug-induced ANCA-associated vasculitis is more favorable compared to the prognosis of idiopathic ANCA-associated vasculitis.
Physicians that are treating patients with vasculitis should be aware of the possible role of drugs and vaccines in the development ANCA-associated vasculitis.
{"title":"Drug- and vaccine induced ANCA-associated vasculitis: An overview","authors":"Jan Willem Cohen Tervaert","doi":"10.1016/j.autrev.2025.103924","DOIUrl":"10.1016/j.autrev.2025.103924","url":null,"abstract":"<div><div>Many different drugs and/or vaccines may cause vasculitis which can be sometimes very severe.</div><div>The clinical presentation varies from isolated skin vasculitis to multi-organ involvement with pulmonary-renal manifestations and/or cerebral vasculitis.</div><div>Whereas causality is difficult to prove and rechallenges are considered unethical, pathophysiological mechanisms suggesting causality have been demonstrated for drugs such as hydralazine, propylthiouracil, levamisole, and immune checkpoint inhibitors.</div><div>An important pathophysiological mechanism of drug-induced anti-neutrophil autoantibody (ANCA)-associated vasculitis is the fact that several drugs have been demonstrated to increase the formation of neutrophil extracellular traps which may result in the development of autoimmunity.</div><div>The first step in medical management of drug-induced ANCA-associated vasculitis is discontinuation of the offending drug and a transparent discussion with the patient regarding the possibility that the drug or the vaccine may have caused vasculitis. Additional treatment with steroids and immunosuppressants is often needed in more severe cases of ANCA-associated vasculitis. In general, however, the long-term prognosis of drug-induced ANCA-associated vasculitis is more favorable compared to the prognosis of idiopathic ANCA-associated vasculitis.</div><div>Physicians that are treating patients with vasculitis should be aware of the possible role of drugs and vaccines in the development ANCA-associated vasculitis.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103924"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487544","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103940
Laxmikausthubha Yaratha, Anushka Deogaonkar, Marie L. Borum
{"title":"Extending the discussion: Cannabis based therapies in inflammatory bowel disease a letter to the editor","authors":"Laxmikausthubha Yaratha, Anushka Deogaonkar, Marie L. Borum","doi":"10.1016/j.autrev.2025.103940","DOIUrl":"10.1016/j.autrev.2025.103940","url":null,"abstract":"","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103940"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145408021","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103953
Frank Verhoeven , Dalil Hannani , Céline Demougeot , Frédéric Meyer , Daniel Wendling , Clément Prati , Athan Baillet
Interleukin-33 (IL-33), an alarmin released upon tissue stress or damage, has gained increasing interest in the pathophysiology of inflammatory diseases such as spondyloarthritis (SpA). Acting through its receptor ST2, IL-33 contributes to the activation of type 2 innate lymphoid cells, Th17 responses, and macrophage polarization. It is involved in key musculoskeletal features of SpA, including enthesitis, synovitis, and axial inflammation, and may also play a role in associated extra-articular manifestations such as gut, skin, eyes inflammation. Preclinical studies targeting the IL-33/ST2 axis have shown promising results, with a reduction of arthritis severity, structural joint damage, and inflammation. The dual role of IL-33 in inflammation and bone metabolism further supports its relevance in SpA. Depending on the cellular context, IL-33 can inhibit osteoclast differentiation or promote pathological bone formation, particularly through the induction of pro-osteogenic macrophages. These findings open the possibility of targeting IL-33 not only to control inflammation but also to modulate structural outcomes, including new bone formation. As current biologics such as anti-TNFα or anti-IL-17 therapies do not fully prevent structural progression in all patients, IL-33 represents an attractive complementary target. This review discusses the emerging role of the IL-33/ST2 pathway in SpA and its potential therapeutic implications.
{"title":"IL-33 in Spondyloarthritis, the missing key","authors":"Frank Verhoeven , Dalil Hannani , Céline Demougeot , Frédéric Meyer , Daniel Wendling , Clément Prati , Athan Baillet","doi":"10.1016/j.autrev.2025.103953","DOIUrl":"10.1016/j.autrev.2025.103953","url":null,"abstract":"<div><div>Interleukin-33 (IL-33), an alarmin released upon tissue stress or damage, has gained increasing interest in the pathophysiology of inflammatory diseases such as spondyloarthritis (SpA). Acting through its receptor ST2, IL-33 contributes to the activation of type 2 innate lymphoid cells, Th17 responses, and macrophage polarization. It is involved in key musculoskeletal features of SpA, including enthesitis, synovitis, and axial inflammation, and may also play a role in associated extra-articular manifestations such as gut, skin, eyes inflammation. Preclinical studies targeting the IL-33/ST2 axis have shown promising results, with a reduction of arthritis severity, structural joint damage, and inflammation. The dual role of IL-33 in inflammation and bone metabolism further supports its relevance in SpA. Depending on the cellular context, IL-33 can inhibit osteoclast differentiation or promote pathological bone formation, particularly through the induction of pro-osteogenic macrophages. These findings open the possibility of targeting IL-33 not only to control inflammation but also to modulate structural outcomes, including new bone formation. As current biologics such as anti-TNFα or anti-IL-17 therapies do not fully prevent structural progression in all patients, IL-33 represents an attractive complementary target. This review discusses the emerging role of the IL-33/ST2 pathway in SpA and its potential therapeutic implications.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103953"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367411","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103984
Ruiying Wang , Xian Wen Tan , Chunyan Yu , Min Li , Siyu Wang , Bingshu Yuan , Xiaoxuan Ma , Qingping Liu , Eiji Matsuura , Lianhua Shen
Beta-2 glycoprotein I (β2GPI) as a core target antigen of antiphospholipid antibodies (aPLs), is a multifunctional plasma protein with phospholipid-binding properties. Under physiological conditions, β2GPI not only binds to negatively charged phospholipids via its domain V but also interacts with various molecules, such as angiostatin4.5 (AS4.5) and annexin II. These interactions play key roles in maintaining the balance between procoagulant and anticoagulant processes and in promoting angiogenesis. β2GPI binds to pathophysiological ligands, such as apoptotic cells, oxidized low-density lipoprotein (oxLDL) and neutrophil extracellular traps (NETs). These complexes can trigger the production of anti-β2GPI autoantibodies in autoimmune patients, leading to antiphospholipid syndrome (APS). The resulting IgG immune complexes activate and impair endothelial cells, resulting in aberrant activation of the coagulation cascade, disruption of lipid metabolic homeostasis, and breakdown of immune tolerance. Together, these processes promote thrombotic events in APS and accelerate the progression of atherosclerotic plaques. This review paper summaries the dynamic conformational transitions of β2GPI's functional domains that elucidates the dual regulatory role of β2GPI-mediated molecular interactions in thrombosis and atherosclerosis (AS) and reveals the mechanism by which anti-β2GPI autoantibodies mediate endothelial injury, thrombosis, and inflammatory amplification. These findings may provide a theoretical molecular basis for the development of novel diagnostic and therapeutic strategies targeting β2GPI.
Take home message
•
β2GPI maintains the balance between procoagulant and anticoagulant processes and regulates angiogenesis.
•
Under pathological conditions, immune complexes of β2GPI with multiple molecules such as PS, oxLDL and PF4 drive the pathological cascade of endothelial damage-thrombosis-inflammatory amplification.
•
Dual-domain targeting (e.g., for stabilizing of DI-DV interaction) to mask antigenicity of β2GPI is potentially useful for inhibiting pathogenic antibody production.
{"title":"The regulatory roles of Beta-2 glycoprotein I (β2GPI) in thrombosis and hemostasis and abnormal disease conditions developed by autoantibodies against β2GPI","authors":"Ruiying Wang , Xian Wen Tan , Chunyan Yu , Min Li , Siyu Wang , Bingshu Yuan , Xiaoxuan Ma , Qingping Liu , Eiji Matsuura , Lianhua Shen","doi":"10.1016/j.autrev.2025.103984","DOIUrl":"10.1016/j.autrev.2025.103984","url":null,"abstract":"<div><div>Beta-2 glycoprotein I (β2GPI) as a core target antigen of antiphospholipid antibodies (aPLs), is a multifunctional plasma protein with phospholipid-binding properties. Under physiological conditions, β2GPI not only binds to negatively charged phospholipids via its domain V but also interacts with various molecules, such as angiostatin4.5 (AS4.5) and annexin II. These interactions play key roles in maintaining the balance between procoagulant and anticoagulant processes and in promoting angiogenesis. β2GPI binds to pathophysiological ligands, such as apoptotic cells, oxidized low-density lipoprotein (oxLDL) and neutrophil extracellular traps (NETs). These complexes can trigger the production of anti-β2GPI autoantibodies in autoimmune patients, leading to antiphospholipid syndrome (APS). The resulting IgG immune complexes activate and impair endothelial cells, resulting in aberrant activation of the coagulation cascade, disruption of lipid metabolic homeostasis, and breakdown of immune tolerance. Together, these processes promote thrombotic events in APS and accelerate the progression of atherosclerotic plaques. This review paper summaries the dynamic conformational transitions of β2GPI's functional domains that elucidates the dual regulatory role of β2GPI-mediated molecular interactions in thrombosis and atherosclerosis (AS) and reveals the mechanism by which anti-β2GPI autoantibodies mediate endothelial injury, thrombosis, and inflammatory amplification. These findings may provide a theoretical molecular basis for the development of novel diagnostic and therapeutic strategies targeting β2GPI.</div></div><div><h3>Take home message</h3><div><ul><li><span>•</span><span><div>β2GPI maintains the balance between procoagulant and anticoagulant processes and regulates angiogenesis.</div></span></li><li><span>•</span><span><div>Under pathological conditions, immune complexes of β2GPI with multiple molecules such as PS, oxLDL and PF4 drive the pathological cascade of endothelial damage-thrombosis-inflammatory amplification.</div></span></li><li><span>•</span><span><div>Dual-domain targeting (e.g., for stabilizing of DI-DV interaction) to mask antigenicity of β2GPI is potentially useful for inhibiting pathogenic antibody production.</div></span></li></ul></div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103984"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896192","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}
Pub Date : 2026-01-01DOI: 10.1016/j.autrev.2025.103937
Joana Gameiro , Martin Windpessl , Patrícia Domingues , Andreas Kronbichler
Rituximab (RTX) is a monoclonal antibody targeted against the B-cell surface antigen CD20 that plays a significant role in the treatment of glomerular diseases. It is approved for the induction and maintenance of remission of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and it is used as off-label treatment in several other diseases. Despite the increased use, there is a lack of high-quality evidence for some indications. More specifically, the optimal initial dosing and subsequent frequency of administration, if even indicated, remain to be established. There are short and long-term risks associated with its use, including serious infectious complications, late-onset neutropenia, sustained B-cell depletion, hypogammaglobulinemia, and impaired response to vaccines. In this review, we aimed to summarize the indications for RTX use in the management of glomerular diseases, addressed the potential risks of this treatment, and highlighted some knowledge gaps which are unlikely to be answered in future clinical trials. While newer B-cell targeting therapies, including CD20-depleting antibodies, are tested and might be more effective or approved based on randomized controlled trials, RTX will remain relevant due to the limited costs to healthcare providers, the good safety profile and the long-standing experience of glomerular disease physician to use it.
{"title":"Rituximab in glomerular diseases: Indications, long-term use, complications and research gaps","authors":"Joana Gameiro , Martin Windpessl , Patrícia Domingues , Andreas Kronbichler","doi":"10.1016/j.autrev.2025.103937","DOIUrl":"10.1016/j.autrev.2025.103937","url":null,"abstract":"<div><div>Rituximab (RTX) is a monoclonal antibody targeted against the B-cell surface antigen CD20 that plays a significant role in the treatment of glomerular diseases. It is approved for the induction and maintenance of remission of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and it is used as off-label treatment in several other diseases. Despite the increased use, there is a lack of high-quality evidence for some indications. More specifically, the optimal initial dosing and subsequent frequency of administration, if even indicated, remain to be established. There are short and long-term risks associated with its use, including serious infectious complications, late-onset neutropenia, sustained B-cell depletion, hypogammaglobulinemia, and impaired response to vaccines. In this review, we aimed to summarize the indications for RTX use in the management of glomerular diseases, addressed the potential risks of this treatment, and highlighted some knowledge gaps which are unlikely to be answered in future clinical trials. While newer B-cell targeting therapies, including CD20-depleting antibodies, are tested and might be more effective or approved based on randomized controlled trials, RTX will remain relevant due to the limited costs to healthcare providers, the good safety profile and the long-standing experience of glomerular disease physician to use it.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103937"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273535","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}
Pub Date : 2026-01-01DOI: 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.
{"title":"Impact of GLP-1 analogues on immune-mediated inflammatory diseases: A systematic review","authors":"Chhagan L. Birda , Fadwa Ibrahim , Abhirup Chatterjee , Anuraag Jena , Vishal Sharma , 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}
Pub Date : 2026-01-01DOI: 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.
{"title":"Sex-specific mechanisms in the pathogenesis and progression of chronic kidney disease","authors":"Guangtao Li , Zhiwei Xu , Hongxia Yang , Dan Zhang , Bin Liu , Yifan Song , Qianhui Li , Yanghe Zhang , Honglan Zhou , 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}
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.
{"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 , Joana Marques-Soares , Enrique Esteve-Valverde , Ariadna Anunciación-Llunell , Catalina Andrada , Monika Ockova , Ariella Hoxha , Munther A. Khamashta , Yehuda Shoenfeld , 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}
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