Autoimmunity reviews最新文献

{"title":"Animal models for connective tissue disease-associated interstitial lung disease: Current status and future directions","authors":"Ziyi Tang ,&nbsp;Hang Yang ,&nbsp;Xiuping Liang ,&nbsp;Jiehao Chen ,&nbsp;Qi He ,&nbsp;Dezhi Zhu ,&nbsp;Yi Liu","doi":"10.1016/j.autrev.2025.103919","DOIUrl":"10.1016/j.autrev.2025.103919","url":null,"abstract":"<div><div>Interstitial lung disease (ILD) significantly contributes to connective tissue disease (CTD) mortality. Although guidelines for managing CTD-associated ILD (CTD-ILD) exist, many patients respond poorly to treatment owing to two key factors: (1) incomplete understanding of subtype-specific pathogenic mechanisms, and (2) reliance on therapies adapted from systemic sclerosis or nonpulmonary rheumatic diseases, which fail to address the unique pathophysiology of distinct CTD-ILD subtypes. This hinders personalized treatment and underscores the need for robust preclinical models that accurately replicate disease-specific mechanisms. However, challenges remain: (1) the lack of models that fully capture the heterogeneity of these disorders and (2) the absence of systematic structured reviews to guide model selection, despite recent advancements in experimental methodologies. These issues often result in mismatches between research goals and model utility.</div><div>This review summarizes current CTD-ILD animal models, focusing on their construction, characteristics, and limitations, and highlighting differences between each model and the corresponding human disease. We summarize these disparities and propose emerging technologies, including CRISPR/Cas9<strong>-</strong>mediated genome editing, humanized mice, and lung organoids/lung-on-a-chip systems, that may facilitate the development of next-generation models. By integrating established and emerging strategies, we aim to provide guidance for model selection and development, promote precision modeling, accelerate targeted therapy discovery, and ultimately improve clinical outcomes. We emphasize the importance of developing subtype-specific models to avoid a “one-model-fits-all” approach.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103919"},"PeriodicalIF":8.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913490","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":"The effect of Sphingosine-1-phosphate receptor modulator treatment on leukocyte subsets across different clinical indications: A systematic review","authors":"Dimitrios Nikolakis ,&nbsp;Christoph Teichert ,&nbsp;Joep Grootjans ,&nbsp;Marleen G.H. van de Sande ,&nbsp;Geert R. D’Haens","doi":"10.1016/j.autrev.2025.103934","DOIUrl":"10.1016/j.autrev.2025.103934","url":null,"abstract":"<div><h3>Background</h3><div>Sphingosine-1-phosphate receptor (S1PR) modulators are approved as a treatment for several autoimmune diseases. While their role on total leukocyte populations is well-studied, their effects on specific leukocyte subsets remain unclear. This systematic review describes the impact of various S1PR modulators on human leukocyte subpopulations.</div></div><div><h3>Methods</h3><div>We conducted a systematic literature search through the databases PubMed, Medline, Embase, and Cochrane, up to the 25th of July 2024. Studies were included if they involved patients treated with S1PR modulators and provided data on leukocyte subsets. Among the exclusion criteria, were non-English articles, animal studies, and in vitro studies. Data extraction focused on changes in leukocyte subsets post-treatment.</div></div><div><h3>Results</h3><div>Out of 1658 articles identified, 63 met the inclusion criteria. Fingolimod was the most frequently studied agent and displayed significant reductions in total T-cell counts. More specifically, CD4+ T-cells, including naïve and central memory populations were reduced. CD8+ T-cells also decreased, although the alterations of effector memory subsets were inconsistent. B-lymphocytes were generally attenuated. Innate immune cells showed variable responses, with most studies indicating a reduction or no change. Data on other S1PR modulators suggested similar trends.</div></div><div><h3>Conclusion</h3><div>S1PR modulators primarily reduce T- and B-cell subpopulations, which are known to play a prominent role in immune-mediated inflammatory disorders. Further research is needed to fully elucidate the differential effects among drugs targeting specific isoforms of the S1PR, focusing on the lymph nodes or inflammatory tissue sites (e.g. intestinal mucosa and cerebrospinal fluid), to explore the exact clinical implications of these pharmacodynamic findings.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103934"},"PeriodicalIF":8.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051547","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":"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}

{"title":"The assessment and management of bone health in pediatric-onset rheumatological diseases from early age to adulthood: A critical overview","authors":"Raffaele Di Taranto ,&nbsp;Andrea Amati ,&nbsp;Chiara Crotti ,&nbsp;Francesco Baldo ,&nbsp;Stefania Costi ,&nbsp;Achille Marino ,&nbsp;Massimo Varenna ,&nbsp;Roberto Caporali ,&nbsp;Cecilia Beatrice Chighizola","doi":"10.1016/j.autrev.2025.103886","DOIUrl":"10.1016/j.autrev.2025.103886","url":null,"abstract":"<div><div>Despite the advancements achieved in modern rheumatology, patients with pediatric-onset rheumatological diseases are still exposed to systemic and/or articular inflammation and corticosteroid treatment, all exerting detrimental effects on the growing skeleton together with the reduced body weight and scarce physical activity that rheumatological patients usually experience. The assessment of bone mass in pediatric subjects carries computational limitations: Dual energy X-ray Absiorptiometry (DXA) underestimates bone mineral density (BMD) especially in case of smaller bone, an instance that occurs frequently in children with rheumatologic conditions due to the high rate of short stature or pubertal delay. The rates of low BMD in juvenile idiopathic arthritis (JIA) patients range between 3 % and 34 %, being higher in systemic and polyarticular JIA; patients with juvenile onset systemic lupus erythematosus (jSLE) present a low BMD in approximately 1/3 of cases. Such reduction in BMD presents early on disease course, persists with aging but might be reversed by rheumatological treatment. In pediatric populations, the term osteoporosis should be reserved to children with clinically relevant fractures, favoring “low BMD for chronological age”. The prevalence of vertebral fractures ranges between 10 % and 30 % in JIA, peaking in female JIA patients aged 10–15 years, and between 21.4 % and 52 % in jSLE. While calcium and vitamin D supplementation should be optimized in all pediatric patients with rheumatological conditions, bisphosphonates should be reserved to subjects with fragility fractures; the prescription for primary fracture prevention in glucocorticoid-treated children is recommended only in case of a dosage &lt;0.1 mg/kg/day for at least 3 months.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103886"},"PeriodicalIF":9.2,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681926","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":"Neutrophil extracellular traps and neuropsychiatric lupus: Signaling pathways involved in NET formation and mechanisms affecting the central nervous system","authors":"Xin Guan,&nbsp;Xiaojie He,&nbsp;Lingjuan Liu","doi":"10.1016/j.autrev.2025.103897","DOIUrl":"10.1016/j.autrev.2025.103897","url":null,"abstract":"<div><div>Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication of systemic lupus erythematosus (SLE) that affects the central or peripheral nervous system. The clinical management of NPSLE faces significant challenges due to the absence of specific diagnostic biomarkers and the lack of standardized, evidence-based diagnostic and therapeutic protocols. Therefore, a comprehensive understanding of the pathogenesis of NPSLE and the exploration of novel therapeutic targets have become urgent priorities in current research. Recent studies have demonstrated that neutrophils and their hallmark product, neutrophil extracellular traps (NETs), play a central role in various pathological processes of NPSLE, with blood-brain barrier (BBB) disruption and the subsequent inflammatory cascade being particularly critical. This paper provides a systematic review of the molecular regulatory network of neutrophils in NPSLE, focusing on the mechanisms by which neutrophils mediate neuroimmune microenvironmental disorders through BBB damage, with the goal of offering a theoretical foundation for the precise diagnosis and treatment of this disease.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103897"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768336","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":"Understanding the effects of Janus kinase inhibitors on the cardiovascular system in comparison to main biological DMARDs in rheumatoid arthritis","authors":"Aliki Zavoriti,&nbsp;Pierre Miossec","doi":"10.1016/j.autrev.2025.103892","DOIUrl":"10.1016/j.autrev.2025.103892","url":null,"abstract":"<div><div>Rheumatoid arthritis (RA) is linked to increased cardiovascular (CV) risk, as is typical for systemic inflammation. The systemic effects of inflammatory cytokines induce vascular dysfunction, leading to thrombosis and other CV diseases. Reducing inflammation should attenuate this risk. For several decades, biologics against a single cytokine, such as TNF inhibitors and IL-6 receptor blockers seem to support this, demonstrating excellent control of RA and reduction of CV events. The Janus kinase inhibitors (JAKi) have been approved more recently. By inhibiting the JAK-STAT pathway, they can simultaneously block the function of multiple cytokines. Unlike biologics, JAKi are associated with increased risk of adverse CV events in high-risk RA patients. This review suggests biological mechanisms that could explain the worse CV outcomes with JAKi compared to biologics. Among the key pro-inflammatory cytokines, IFNγ, IL-6 and IL-23 use directly the JAK-STAT pathway, whereas IL-17, TNF and IL-1β do not, lacking JAK-related receptors. Nevertheless, these non-JAK-dependent cytokines can still influence the JAK-STAT pathway to promote vascular effects in an indirect fashion. Moreover, IL-17 and TNF specifically when combined, exert major pro-coagulant and pro-thrombotic effects on vessels independently of JAKs. As a result, JAKi might not block these pathways and even upregulate them, at high concentrations, leading to increased thrombotic risk. Finally, new research shows that JAKi cannot prevent the increase in adhesion and coagulation molecules as well as the deficiency in physiological anti-coagulant proteins triggered by TNF and IL-17 on endothelial cells. Increased efforts to control CV risk factors are critical in this context.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103892"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726966","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":"Unmet needs and emerging pharmacotherapies for autoimmune connective tissue disease-associated interstitial lung diseases","authors":"Yasuhiro Kondoh ,&nbsp;Takao Fujii ,&nbsp;Yoshikazu Inoue ,&nbsp;Tatsuya Atsumi","doi":"10.1016/j.autrev.2025.103900","DOIUrl":"10.1016/j.autrev.2025.103900","url":null,"abstract":"<div><div>Autoimmune connective tissue disease associated with interstitial lung disease (CTD-ILD) includes rheumatoid arthritis-associated ILD, systemic sclerosis-associated-ILD, and several other ILDs. Many patients with CTD-ILD—as well as individuals with other ILDs—develop a progressive pulmonary fibrosis (PPF) similar to idiopathic pulmonary fibrosis (IPF). PPF is characterized by worsening respiratory symptoms, declining lung function despite current pharmacotherapies, and ultimately early death. Current pharmacotherapies for CTD-ILD and PPF include glucocorticoids, immunosuppressants, and anti-fibrotic agents. Due to the scarcity of randomized clinical trials for CTD-ILD, many pharmacotherapies are generally administered off-label (although several are approved in Japan), with notable exceptions including nintedanib, an anti-fibrotic agent approved for SSc-ILD and chronic progressive fibrosing ILD in several countries. As the available agents only slow the decline of pulmonary function and are associated with treatment-limiting side effects, there is a need for more efficacious and tolerable pharmacotherapies for CTD-ILD and PPF. Promising compounds in clinical trials include nerandomilast (a preferential phosphodiesterase 4B inhibitor), admilparant (a lysophosphatidic acid receptor 1 antagonist), and inhaled treprostinil (a prostacyclin analogue). Nerandomilast may have both anti-fibrotic and immunomodulatory properties; in preclinical models of PPF, it reduced neutrophils and macrophages and down-regulated pro-fibrotic signaling pathways. Hopefully, therefore, this pipeline will produce new medications to ease the collectively large burden of CTD-ILD and PPF.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103900"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793369","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":"Monoclonal Gammopathy of Rheumatologic Significance (MGRhS): a systemic vision of clonal disorders with multiple organ involvement","authors":"Luca Quartuccio ,&nbsp;Valeria Manfrè ,&nbsp;Elena Treppo ,&nbsp;Fabio Perrotta ,&nbsp;Gaafar Ragab ,&nbsp;Andreas Goules ,&nbsp;Ennio Lubrano","doi":"10.1016/j.autrev.2025.103895","DOIUrl":"10.1016/j.autrev.2025.103895","url":null,"abstract":"<div><div>Monoclonal gammopathy (MG) encompasses a spectrum of conditions ranging from benign to malignant clonal B-cell proliferations. While MG is traditionally associated with hematologic malignancies, its role in autoimmune and rheumatologic diseases is increasingly recognized. This review proposes the novel concept of <em>“monoclonal gammopathy of rheumatologic significance (MGRhS)”</em> that refers to a non-malignant or pre-malignant systemic condition related to a monoclonal immunoglobulin and clonal B cells, capable of producing multi-organ damage or influencing the therapeutic management of rheumatologic diseases.</div><div>MG of clinical significance is characterized by the production of monoclonal proteins causing organ damage and modulating immune responses. These proteins contribute to rheumatologic conditions or peculiar phenotypes, including cryoglobulinemic vasculitis, Sjögren's disease, and other autoimmune disorders. The review explores pathogenic mechanisms linking MG with these diseases, emphasizing early detection and accurate classification to guide therapeutic strategies.</div><div>The manuscript addresses the implications of incidental MG detection in rheumatologic patients, particularly in the context of biologic therapies. Practical guidance is provided on identifying MGRhS, assessing its impact, and tailoring management to prevent complications.</div><div>This analysis aims to advance understanding of MGRhS as a distinct clinical entity, encouraging a multidisciplinary approach to its management. The integration of novel diagnostic tools and targeted therapies is essential to improve outcomes and address the complexity of this condition.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103895"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759028","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":"Systemic auto-inflammatory diseases, auto-immune diseases and immune deficiencies: From independent to overlapped diseases approach","authors":"Anne-Sophie Parentelli ,&nbsp;Anne-Aurélie Lopes ,&nbsp;Frédéric Rieux-Laucat ,&nbsp;Olivier Hermine","doi":"10.1016/j.autrev.2025.103901","DOIUrl":"10.1016/j.autrev.2025.103901","url":null,"abstract":"<div><div>Systemic AutoInflammatory Diseases (SAIDs), AutoImmune Diseases (AIDs), and Primary Immune Deficiencies (PIDs) were formely considered independent, even opposing, conditions. SAIDs were associated with the innate immune system, involving dysregulation of inflammation and recurrent episodes of systemic inflammation without an infectious process. Their original definition did not involve autoreactive cells or autoantibodies. In contrast, PIDs were characterised by defects in the adaptive or innate immune system, leading to recurrent infections and immune dysfunction. AIDs were inflammatory diseases also characterised by dysregulation of the immune system attacking its own tissues through autoreactive cells or autoantibodies. Nevertheless, advancements in genetics and a deeper understanding of T-cell development and signalling, immune tolerance, the complement pathway and inflammation have revealed that these conditions are overlapping diseases with shared immune system dysfunctions. These diseases now represent a continuum within a broader spectrum of disorders known as “Inborn Errors of Immunity”. However, this term is not suitable as it does not fully encompass cases arising from somatic mutations and can be stigmatising for patients. Therefore, we propose the terms “Primary Immune Deficiencies and Dysregulations” (PIDDs) or simply “Primary Immune Disorders” (PIDs) as more appropriate alternatives.</div><div>Thus, this article aims to describe known diseases where autoimmunity, autoinflammation and primary immunodeficiencies overlap, along with some mechanisms that may explain these interconnections. To our knowledge, no comprehensive reviews on this topic currently exist, despite its significance in modifying our understanding of these diseases, their treatment, and associated research.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103901"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793368","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":"Cognitive impairment in systemic autoimmune and inflammatory diseases: A narrative review focused on ANCA-associated vasculitis, sarcoidosis, Sjögren's syndrome, systemic sclerosis, and Behçet's disease","authors":"Marion Camard ,&nbsp;Fanny Urbain ,&nbsp;Nicolas Noel","doi":"10.1016/j.autrev.2025.103899","DOIUrl":"10.1016/j.autrev.2025.103899","url":null,"abstract":"<div><div>Cognitive impairment is an increasingly recognized feature of systemic autoimmune and inflammatory diseases, yet remains underdiagnosed and insufficiently studied beyond systemic lupus erythematosus. In this narrative review, we explore the prevalence, clinical profiles, and pathophysiological mechanisms of cognitive dysfunction in five systemic diseases: ANCA-associated vasculitis (AAV), primary Sjögren's syndrome (pSS), systemic sclerosis (SSc), sarcoidosis, and Behçet's disease (BD). We conducted a structured literature search in PubMed and Embase to identify relevant studies published between 1954 and 2024. Reported prevalence varies widely: ∼30 % in AAV, 0–35 % in sarcoidosis, 10–80 % in pSS, 8–65 % in SSc, and 30–100 % in BD. Executive dysfunction and attention deficits predominate. In some cases—particularly in AAV and BD—cognitive decline may reflect direct central nervous system involvement, but many patients report cognitive complaints without overt neurological manifestations or imaging abnormalities. Proposed mechanisms include blood-brain barrier disruption, cytokine-driven neuroinflammation (notably IL-6, TNF-α, IFN-γ, BAFF), autoantibody-mediated synaptic toxicity, and cerebral hypoperfusion linked to small-vessel vasculopathy. Glial activation and neuroimmune dysregulation are recurring findings in animal models and functional imaging studies. White matter lesions and abnormal brain perfusion on MRI or SPECT are frequently observed in asymptomatic patients. Comorbid symptoms such as depression, fatigue, pain, and small fiber neuropathy may exacerbate or mimic cognitive dysfunction. Despite its prevalence and impact on quality of life, cognitive dysfunction is rarely screened, partly due to a lack of standardized tools. Harmonized neurocognitive assessment protocols and longitudinal studies are urgently needed to improve understanding, detection, and management of cognitive impairment, and support its integration into routine care.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103899"},"PeriodicalIF":8.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793367","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}