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":"2025-08-25","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":"Systemic sclerosis and AHR: Shedding light on a hidden connections","authors":"Anna Wajda ,&nbsp;Agnieszka Paradowska-Gorycka ,&nbsp;Charlotte Esser","doi":"10.1016/j.autrev.2025.103915","DOIUrl":"10.1016/j.autrev.2025.103915","url":null,"abstract":"<div><div>Systemic sclerosis (SSc) is a complex and debilitating autoimmune disease marked by fibrosis of the skin and inner organs, alongside chronic inflammation, and vascular abnormalities. SSc pathogenesis involves both genetic and environmental factors, such as silica dust or benzene exposure but the underlying molecular mechanisms regulating fibrogenesis and organ involvement are not fully understood. In part due to this knowledge gap, treatment options are limited. In this review we look at the possible role of the aryl hydrocarbon receptor (AHR), a transcription factor involved in immunomodulation, fibrosis and drug metabolism and inflammatory responses, especially in barrier organs. AHR activation by binding to one of its many small molecular weight ligands can result in gene-expression changes in the nucleus (its role as a transcription factor) but also lead to knock-on effects on other signaling pathways via direct binding (e.g., to NFkB) or via AHR's protein degradation capacity (E3 ligase). In some cell types transcription target genes include the fibrogenic cytokine TGF-β or metalloproteinases responsible for extracellular matrix remodeling. AHR has been shown to be highly expressed in all cutaneous cell populations, and to be critical for skin homeostasis. Given its context-dependent effects, AHR may act as both a pro- and anti-fibrotic regulator in SSc, depending on ligand availability and cellular environment. This dual role highlights AHR as a potential therapeutic target, where selective agonists or antagonists could help restore immune and fibrotic homeostasis. Here, we explore these mechanisms and discuss the potential of AHR as a therapeutic target for modulating disease progression and improving patient outcomes.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103915"},"PeriodicalIF":8.3,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903205","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":"In search of biomarkers for prediction of drug treatment responses in rheumatoid arthritis: Lessons learned and future perspectives","authors":"Athanasia Dara,&nbsp;Nikolaos I. Vlachogiannis,&nbsp;George E. Fragoulis,&nbsp;Maria G. Tektonidou,&nbsp;Petros P. Sfikakis","doi":"10.1016/j.autrev.2025.103914","DOIUrl":"10.1016/j.autrev.2025.103914","url":null,"abstract":"<div><div>Prompt initiation of effective drug treatment is crucial for controlling inflammation and preventing disease progression in rheumatoid arthritis, the most prevalent systemic rheumatic disease. The growing range of drug therapies over the past three decades and the fact that only a minority of patients achieve sustained long-term remission with any given therapy, make imperative the need for biomarkers predicting responses to specific drugs. Moreover, promising therapeutic approaches under development, namely cellular therapies, could be promptly applicable at earlier disease stages in about 10-15 % of RA patients who will be refractory to all approved drugs. In this scoping review of original articles published until 25th of July 2025, we present a critical overview of the literature pertaining to the prognostic value of blood immunophenotyping, circulating proteins and blood proteomics, transcriptomics, metabolomics and lipidomics, as well as of endogenous cortisol production and synovial histopathology. We also discuss the emerging use of artificial intelligence-based approaches for developing response prediction models that integrate clinical features with molecular profiling. We conclude that current knowledge does not allow to discern future responders to methotrexate and/or to different biologic agents from non-responders because established biomarkers to identify those patients who will benefit the most from each therapeutic option are lacking. We also emphasize the lack of standardized research approaches to discover biomarkers predicting drug treatment responses and try to identify the relevant pitfalls and describe the lessons learned over the years. Finally, we propose a roadmap and the application of advanced analytical and machine learning techniques for future research in this area.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103914"},"PeriodicalIF":8.3,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908576","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":"Rapid radiographic progression in rheumatoid arthritis: Definition, prediction and treatment","authors":"Bo Lv ,&nbsp;Fanshu Li ,&nbsp;Fanlei Hu ,&nbsp;Liling Xu","doi":"10.1016/j.autrev.2025.103913","DOIUrl":"10.1016/j.autrev.2025.103913","url":null,"abstract":"<div><div>Rapid radiographic progression (RRP) in rheumatoid arthritis (RA) is strongly correlated with unfavorable long-term prognostic outcomes. Early identification of RRP is paramount, as prompt intervention and the implementation of intensified therapeutic regimens have the potential to substantially improve clinical outcomes. This review summarized the different definitions and current key predictors of RRP, such as genetic predispositions, body mass index and so on. Furthermore, the existing matrix-based predictive models for RRP were compared. In addition, the potential treatment options for patients with RRP were also outlined. The objective of this review is to improve the early detection of RRP, thereby facilitating timely intervention and the adoption of personalized treatment paradigms that optimize patient prognosis.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 10","pages":"Article 103913"},"PeriodicalIF":8.3,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881967","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 lupus erythematosus in critical care: A systematic review of ICU outcomes and management","authors":"Edith Ramírez-Lara ,&nbsp;Claudia Mendoza-Pinto ,&nbsp;Pamela Munguía-Realpozo ,&nbsp;Miguel Ángel Saavedra-Salinas ,&nbsp;Ivet Etchegaray-Morales ,&nbsp;Jorge Ayón-Aguilar ,&nbsp;Álvaro José Montiel-Jarquín ,&nbsp;Socorro Martínez-Méndez","doi":"10.1016/j.autrev.2025.103911","DOIUrl":"10.1016/j.autrev.2025.103911","url":null,"abstract":"<div><h3>Background</h3><div>Systemic lupus erythematosus (SLE) often progresses to critical illness requiring intensive care unit (ICU) admission, yet contemporary data on outcomes, prognostic factors, and therapeutic approaches are scattered.</div></div><div><h3>Objective</h3><div>To synthesize recent evidence on causes of ICU admission, mortality predictors, and management strategies in adult SLE.</div></div><div><h3>Methods</h3><div>A PRISMA-compliant search of PubMed, Web of Science and Cochrane Library (inception–31 December 2024) retrieved studies enrolling adults (≥18 years) with confirmed SLE treated in ICUs. Two reviewers independently selected articles and extracted data; methodological heterogeneity precluded meta-analysis, so results were narratively synthesized.</div></div><div><h3>Results</h3><div>Thirty-nine studies met the criteria. Infection (40 %), pulmonary involvement (17 %) and renal flares (13 %) were the most common admission triggers. Reported ICU mortality ranged from 20 % to 82 % but rose sharply when baseline Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) exceeded 16, approximating 80 % mortality (sensitivity 84 %, specificity 90 %) and outperforming Acute Physiology and Chronic Health Evaluation (APACHE) II and Sequential Organ Failure Assessment (SOFA) in discriminating survivors. Additional independent predictors were APACHE II &gt; 16, need for mechanical ventilation, renal replacement therapy and vasopressor support. Mechanical ventilation (59 %) and vasoactive agents (39 %) were the predominant ICU interventions. Immunomodulatory management was heterogeneous: high-dose corticosteroids and cyclophosphamide were ubiquitous, whereas mycophenolate, antimalarials, intravenous immunoglobulin, plasmapheresis, and extracorporeal membrane oxygenation were reserved for selected scenarios.</div></div><div><h3>Conclusions</h3><div>Early recognition of poor prognostic factors and prompt ICU admission are essential to improving outcomes in SLE<strong>.</strong></div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103911"},"PeriodicalIF":8.3,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881968","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":"Gut microbiota in rheumatoid arthritis: Mechanistic insights, clinical biomarkers, and translational perspectives","authors":"Xiang-Yu Qi ,&nbsp;Meng-Xia Liu ,&nbsp;Xiao-Jing Jiang ,&nbsp;Tian Gao ,&nbsp;Guo-Qiang Xu ,&nbsp;He-Yi Zhang ,&nbsp;Qin-Yi Su ,&nbsp;Yi Du ,&nbsp;Jing Luo ,&nbsp;Sheng-Xiao Zhang","doi":"10.1016/j.autrev.2025.103912","DOIUrl":"10.1016/j.autrev.2025.103912","url":null,"abstract":"<div><div>Rheumatoid arthritis (RA) is a systemic autoimmune disease shaped by complex interactions between genetics and environmental factors, among which gut microbiota has emerged as a critical modulator. Recent advances have implicated gut microbiota dysbiosis in RA pathophysiology, with evidence spanning mechanistic, diagnostic, and therapeutic dimensions. This review summarizes current knowledge of the gut-joint axis and outlines microbiota-based strategies for RA management. Numerous studies have demonstrated consistent alterations in gut microbial communities in patients with RA, with enrichment of <em>Prevotella copri</em> observed in 75% of patients with new-onset RA compared to 21.4% of healthy controls, suggesting a potential association with disease initiation. Mechanistically, we detail how microbial dysbiosis, including that of bacteria, fungi, and viruses, disrupts intestinal barrier integrity, skews T helper 17/T regulatory and T follicular helper/T follicular regulatory immune axes, induces molecular mimicry, and alters the profiles of microbial metabolites such as short-chain fatty acids. Diagnostically, microbial taxa and metabolites serve as promising biomarkers. Machine learning models based on microbiota profiles have achieved area under the curve (AUC) values exceeding 0.88, with discriminatory taxa such as <em>Ruminococcus gnavus</em> and <em>Fusicatenibacter</em>. Therapeutically, we reviewed microbiota-targeted interventions, such as probiotics, prebiotics, antibiotics, fecal microbiota transplantation, diet, and herbal medicines, highlighting the emerging field of pharmacomicrobiomics. Gut microbial signatures have shown promise in predicting treatment responses, including methotrexate efficacy via the enterotype-based gut microbial human index model (AUC = 0.945). This review proposes an integrated framework linking microbial alterations with RA onset and progression and presents gut microbiota as a promising frontier for biomarker discovery, personalized intervention, and precision medicine.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 12","pages":"Article 103912"},"PeriodicalIF":8.3,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871178","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 mTOR signaling pathway in systemic lupus erythematosus and systemic vasculitis","authors":"Despina Michailidou ,&nbsp;Yevgeniya Gartshteyn ,&nbsp;Anca D. Askanase ,&nbsp;Andras Perl","doi":"10.1016/j.autrev.2025.103910","DOIUrl":"10.1016/j.autrev.2025.103910","url":null,"abstract":"<div><div>The mechanistic target of rapamycin (mTOR) is a central regulator of cellular proliferation, metabolism, survival and growth. The mTOR pathway consists of two protein complexes, mTORC1 and mTORC2, which have different sensitivities to rapamycin and cellular functions. mTOR regulates autophagy as well as the function and/or differentiation of many immune cells, including T cells, dendritic cells, natural killer cells, macrophages, neutrophils, and B cells. mTOR signaling is implicated in the pathogenesis of cancer, diabetes and several autoimmune diseases. In this review, we summarize how mTOR pathway may contribute to the pathogenesis of systemic lupus erythematosus (SLE) and systemic vasculitis. In SLE, mTOR activation induces activation of CD4 + T cells, skews differentiation towards Th17 cells resulting in Th17/Treg imbalance, increases production of IL-4 in CD4 − CD8− double-negative (DN) T cells, reduces the number of circulating CD8⁺ memory T cells, promotes B-cell proliferation, increases production of plasmacytes and secretion of autoantibodies, as well as activation of myeloid dendritic cells. In large vessel vasculitis, mTOR overactivity promotes endothelial cell growth, T cell differentiation towards Th1 and Th17 polarization, impairment of Tregs and activation of smooth muscle cell-derived myofibroblasts that contribute to arterial stenosis and ischemia, whereas in anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, reduced activity of the mTOR signaling pathway is observed in neutrophils isolated during the active phase of the disease. Targeting mTOR pathway with rapamycin, rapalogues, or other mTOR inhibitors could be efficacious in the treatment of these complex autoimmune diseases.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 11","pages":"Article 103910"},"PeriodicalIF":8.3,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144841533","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":"2025-08-06","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":"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":"2025-08-05","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":"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":"2025-08-05","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}