Autoimmunity reviews最新文献

{"title":"LAG-3 in (auto)immunity and cancer - Emphasising its role in antigen presenting cells","authors":"Aleksandra Wiśniewska ,&nbsp;Elżbieta Sarnowska ,&nbsp;Katarzyna Kozak ,&nbsp;Piotr Rutkowski ,&nbsp;Paweł Sobczuk","doi":"10.1016/j.autrev.2026.103992","DOIUrl":"10.1016/j.autrev.2026.103992","url":null,"abstract":"<div><div>The growing popularity of immunotherapy shows a promising future for cancer treatment. However, a significant need to develop new therapeutics that could be successfully used in therapy still remains, especially in “immune-cold” tumors that are not responsive to classic anti-PD-1 treatment. Therefore, the discovery of lymphocyte activation gene-3 (LAG-3) as a new immune checkpoint (IC) molecule that physiologically participates in auto-tolerance mechanisms preventing auto-aggression was a significant milestone in immuno-oncology. Two main approaches aim to introduce LAG-3-directed therapies into clinical practice: anti-LAG-3 antibodies that are meant to inhibit LAG-3 function and recombinant soluble LAG-3 form that aim to activate immune response, especially by interacting with the antigen-presenting cells (APCs). So far, studies show that both approaches may be safe and effective anti-cancer treatment options. This review summarises the role of LAG-3 in immune response and emphasises the role of this IC molecule and its soluble form on APCs function, while also noting the primary physiological function of LAG-3 in autoimmunity and providing a dual perspective of the pros and cons of this novel anti-cancer therapy.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103992"},"PeriodicalIF":8.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050122","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}

{"title":"Gastrointestinal histology of systemic sclerosis: A systematic review","authors":"Aidan K. Strother ,&nbsp;Robert M. Anderton ,&nbsp;Naveen Kalavar ,&nbsp;Ali Y. Ayla ,&nbsp;Tracy Ashby ,&nbsp;Amanda Mayer ,&nbsp;Roshan Dongre ,&nbsp;Francesco Bonomi ,&nbsp;Silvia Bellando Randone ,&nbsp;Michael Hughes ,&nbsp;Zsuzsanna H. McMahan","doi":"10.1016/j.autrev.2026.103988","DOIUrl":"10.1016/j.autrev.2026.103988","url":null,"abstract":"<div><h3>Objective</h3><div>To systematically review and synthesize the histological findings of gastrointestinal (GI) tissue in patients with systemic sclerosis (SSc), aiming to clarify the role of fibrosis and other pathological processes in SSc-related GI disease.</div></div><div><h3>Methods</h3><div>A comprehensive literature search was conducted across MEDLINE (OVID), Web of Science, and Cochrane Library databases for studies published in English from 1960 to 2025. Inclusion criteria required studies to report qualitative histological findings from GI tissue (esophagus to anorectum) in adult SSc patients, excluding those with overlapping autoimmune diseases or malignancy. Data extraction and appraisal were performed independently by multiple reviewers.</div></div><div><h3>Results</h3><div>Of 1697 screened articles, 36 met inclusion criteria. Histological analysis revealed that fibrosis, while common, was not universal nor evenly distributed across GI layers. The mucosa predominantly exhibited inflammatory infiltrates (mast cells, macrophages, lymphocytes), villous atrophy, and less frequent fibrosis. Submucosal findings were inconsistent, with variable reports of vascular changes and nerve plexus degeneration. The muscularis layer showed near-universal smooth muscle atrophy and variable fibrosis, with decreased density of interstitial cells of Cajal (ICC) in some studies. Neuronal and mitochondrial pathology were underreported.</div></div><div><h3>Conclusion</h3><div>GI pathology in SSc is multifaceted, involving inflammation, cellular degeneration, neuronal dysfunction, and smooth muscle atrophy, with fibrosis as a variable feature. Standardization of histological reporting and further ultrastructural studies are needed to elucidate mechanisms and guide future research and therapeutic strategies.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 2","pages":"Article 103988"},"PeriodicalIF":8.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043592","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}

{"title":"Ferritinophagy in inflammatory and autoimmune diseases: Mechanistic insights and therapeutic potentials","authors":"Yi Wang ,&nbsp;Yang Li ,&nbsp;Jiani Jiang ,&nbsp;Yanggang Hong ,&nbsp;Sheng Gao ,&nbsp;Chunyan Hua","doi":"10.1016/j.autrev.2025.103954","DOIUrl":"10.1016/j.autrev.2025.103954","url":null,"abstract":"<div><div>Ferritinophagy, a selective form of autophagy mediated by nuclear receptor coactivator 4 (NCOA4), degrades ferritin to regulate intracellular iron homeostasis and has emerged as an important process in inflammatory and autoimmune diseases. By controlling ferritin turnover, ferritinophagy affects labile iron levels and ferroptosis, an iron-dependent cell death driven by lipid peroxidation, and interacts with multiple immune regulatory pathways. This process is modulated by signaling networks such as MAPK, cGAS-STING, NF-κB, AMPK/mTOR, and NRF2, which link iron metabolism to inflammatory responses. Aberrant ferritinophagy has been implicated in conditions including sepsis, osteoarthritis, asthma, rheumatoid arthritis, and systemic lupus erythematosus. Preclinical studies demonstrate that strategies such as inhibiting the JNK-JUN or cGAS-STING pathways, or applying iron chelators like deferoxamine, can reduce iron overload, limit ferroptosis, and attenuate inflammation. Despite these advances, further work is needed to delineate disease-specific regulatory mechanisms and to translate ferritinophagy modulation into safe and effective therapies. This review summarizes current mechanistic insights and therapeutic prospects, highlighting ferritinophagy as a promising target for managing inflammatory and autoimmune disorders.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103954"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145426344","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}

{"title":"Regulated cell death in systemic lupus erythematosus: Key pathways and targeted therapies","authors":"Siying Deng,&nbsp;Ziwei Hu,&nbsp;Shaozhe Cai,&nbsp;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}

{"title":"Senescent CD4+ T cells and autoimmune diseases: mechanisms and therapeutic prospects","authors":"Yue Hu ,&nbsp;Liting He ,&nbsp;Hai Long","doi":"10.1016/j.autrev.2025.103957","DOIUrl":"10.1016/j.autrev.2025.103957","url":null,"abstract":"<div><div>Senescent CD4⁺ T cells exhibit classical features of T-cell senescence—including telomere attrition, reduced proliferative capacity, and an upregulated senescence-associated secretory phenotype (SASP)—while also displaying unique characteristics. Notably, they maintain relatively healthy mitochondrial mass compared with senescent CD8⁺ T cells, a distinction that influences their roles in immune regulation and tissue pathology. Multiple signaling pathways, such as the ATM–DDR–p53 axis, AMPK–TAB1–p38 cascade, mTOR signaling, mitochondrial–ROS axis, and IL-7/IL-2 cytokine networks, are dysregulated during the senescence of CD4⁺ T cells. Importantly, senescent CD4⁺ T cells can promote chronic inflammation, disrupt immune homeostasis, and remodel tissue microenvironments through the secretion of SASP components (e.g., IL-6, IL-8, TNF-α, and MMPs). They also have the potential to enhance antibody secretion by B cells, ultimately contributing to tissue-specific damage. These aberrant cells have been shown to accumulate in several autoimmune diseases (ADs), including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic sclerosis (SSc). Targeting senescent CD4⁺ T cells with senotherapeutic agents and SASP inhibitors has been shown to markedly suppress AD progression, underscoring the translational potential of this therapeutic approach. However, more specific senescence markers are needed to accurately identify senescent CD4⁺ T cells. This review synthesizes current knowledge on senescent CD4⁺ T cells and their involvement in autoimmune diseases. Future research should prioritize elucidating their pathogenic mechanisms and developing targeted therapeutic strategies to mitigate their detrimental effects in ADs.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 1","pages":"Article 103957"},"PeriodicalIF":8.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145538737","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}

{"title":"Association between weather conditions and rheumatoid arthritis: A systematic review and meta-analysis","authors":"Chao Hu ,&nbsp;Jingyi Wu ,&nbsp;Yuanyuan Luo ,&nbsp;Yichun Zhu,&nbsp;Runyu Chang,&nbsp;Suhai Qian,&nbsp;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 &lt; 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> &lt; 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}

{"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}

{"title":"Extending the discussion: Cannabis based therapies in inflammatory bowel disease a letter to the editor","authors":"Laxmikausthubha Yaratha,&nbsp;Anushka Deogaonkar,&nbsp;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}

{"title":"IL-33 in Spondyloarthritis, the missing key","authors":"Frank Verhoeven ,&nbsp;Dalil Hannani ,&nbsp;Céline Demougeot ,&nbsp;Frédéric Meyer ,&nbsp;Daniel Wendling ,&nbsp;Clément Prati ,&nbsp;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}

{"title":"Rituximab in glomerular diseases: Indications, long-term use, complications and research gaps","authors":"Joana Gameiro ,&nbsp;Martin Windpessl ,&nbsp;Patrícia Domingues ,&nbsp;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}