Autoimmunity reviews最新文献

{"title":"Interleukin-6 in neuroimmunological disorders: Pathophysiology and therapeutic advances with satralizumab","authors":"Xicheng Li ,&nbsp;Chongbo Zhao","doi":"10.1016/j.autrev.2025.103826","DOIUrl":"10.1016/j.autrev.2025.103826","url":null,"abstract":"<div><div>Interleukin-6 (IL-6) is a multifunctional cytokine produced by various cells of the innate and adaptive immune systems. It acts as a regulatory factor in immunity, inflammation, metabolism, and cellular function in multiple organs and systems. The functionality of IL-6 is achieved through multiple signal transduction pathways, such as the JAK/STAT and the NF-κB signaling pathways. In this review, we highlighted the inflammatory and non-inflammatory functions of IL-6, as well as the associated signaling pathways. The involvement of IL-6 in neuroimmunological disorders suggests that the interleukin-6 receptor (IL-6R) monoclonal antibody, satralizumab, is a potential therapeutic strategy. Phase III clinical trials have already validated the safety and efficiency of satralizumab in treating neuromyelitis optica spectrum disorders (NMOSD) and acetylcholine receptor (AChR) seropositive generalized myasthenia gravis (gMG). This review aims to elucidate the pathophysiological role of IL-6, and explore the clinical implications of satralizumab in neuroimmunological diseases, providing insights into its potential therapeutic applications.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103826"},"PeriodicalIF":9.2,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143905881","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 emerging concept of ANCA-associated vasculitis related to inborn errors of immunity","authors":"Clément Triaille ,&nbsp;Benjamin Terrier ,&nbsp;Alice Hadchouel ,&nbsp;Elie Haddad ,&nbsp;Augusto Vaglio ,&nbsp;Marie-Louise Frémond","doi":"10.1016/j.autrev.2025.103824","DOIUrl":"10.1016/j.autrev.2025.103824","url":null,"abstract":"<div><div>ANCA-associated vasculitis (AAV) is a group of rare small vessels vasculitis that preferentially affect the kidneys, lungs and upper airways. Although the detailed pathophysiology remains unclear, genetic background has been shown to play a role in sporadic forms of AAV. The discovery of these susceptibility genes (and associated biological pathways) involved in AAV have shaped the current understanding of AAV pathophysiology. In addition to common genetic polymorphisms, specific rare inborn errors of immunity (IEI) have been described with a high frequency of ANCA (antineutrophil cytoplasmic antibodies) positivity and vasculitis features in young individuals (in addition to other manifestations). A systematic literature search revealed that patients with pathogenic variants in <em>COPA, STING1, DNASE1L3,</em> and <em>PIK3CD</em> are at increased risk of developing ANCA and AAV features, including alveolar hemorrhage, interstitial lung disease, pauciimmune glomerulonephritis, and upper airways involvement (septum perforation, saddle-nose deformity, chronic nasal/sinuses ulceration). Some of these IEI may also present with a mixed phenotype and/or auto-antibodies profile associating features of AAV and other autoimmune diseases (in particular systemic lupus erythematosus). Notably, a proportion of reports and series lack serological (ANCA specificity and titers) and/or histopathological data, making challenging to assess the likelihood for ANCA pathogenicity in some patients with IEI (as opposed to unspecific signs of biologic autoimmunity). This point is nonetheless essential to make appropriate therapeutic decisions. In addition, since most of the genes mentioned above are involved in the type 1 interferon signaling, the role of this pathway in AAV etiopathogenesis deserves further investigation.</div><div>In this review, we will describe these IEI, their overlap with sporadic AAV, and their evocative features. Next, we will discuss how these monogenic conditions might inform our general understanding of AAV pathophysiology. We also propose some directions for future research in order to better define the link between ANCA and IEI. Finally, we will consider how making the diagnosis of an IEI in a patient with AAV features might impact individual management.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103824"},"PeriodicalIF":9.2,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143894301","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":"Coffee consumption and risk of multiple sclerosis: A systematic review and meta-analysis","authors":"Mehrad Amirnia ,&nbsp;Khazar Raeisnia ,&nbsp;Hamidreza Ashayeri ,&nbsp;Zahra Hakimzadeh ,&nbsp;Ehsan Nasiri ,&nbsp;Mahnaz Talebi ,&nbsp;Sarvin Sanaie ,&nbsp;Amirreza Naseri","doi":"10.1016/j.autrev.2025.103822","DOIUrl":"10.1016/j.autrev.2025.103822","url":null,"abstract":"<div><h3>Background</h3><div>Multiple Sclerosis (MS) is an immune-mediated disease with miscellaneous etiological origins. Given caffeine's neuroprotective and anti-inflammatory attributes and its potential influence on MS risk, and to address the conflict in the clinical evidence, this study aims to comprehensively review the existing literature on the association between coffee consumption and the risk of MS.</div></div><div><h3>Methods</h3><div>Following the PRISMA 2020 guidelines, a systematic search in PubMed, Scopus, Web of Science, and Embase for the studies published up to January 2024 was conducted. Studies that assessed the relationship between coffee intake and the risk of MS were included, and reviews, case reports, non-English papers, in vitro and animal studies, and conference abstracts were excluded. The risk of bias was assessed using the JBI checklists, and meta-analyses were conducted based on odds ratio (OR) using the fourth version of CMA software.</div></div><div><h3>Results</h3><div>Out of 604 initial records, 10 observational studies with 19,430 participants met the inclusion criteria. The included case-control studies showed an overall high quality. Meta-analysis revealed a reduction in MS development in coffee consumers both before (OR: 0.66; 95 % CI: 0.49–0.90; <em>p</em>-value: 0.008; I²: 89.65 %; p-value for heterogeneity&lt;0.001) and after adjustment for possible confounders (adjusted OR: 0.42; 95 % CI: 0.20–0.90; p-value: 0.025; I²: 89.65 l; p-value for heterogeneity&lt;0.001).</div></div><div><h3>Conclusion</h3><div>Coffee consumption, may decrease the risk of MS; however, further well-designed prospective studies are required to ascertain this association.</div><div>PROSPERO registration number: CRD42023484298.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103822"},"PeriodicalIF":9.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887886","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":"Rebalancing redox homeostasis: A pivotal regulator of the cGAS-STING pathway in autoimmune diseases","authors":"Yuchen Zhao ,&nbsp;Tianhao Xu ,&nbsp;Zhaoshun Wu ,&nbsp;Ning Li ,&nbsp;Qianqian Liang","doi":"10.1016/j.autrev.2025.103823","DOIUrl":"10.1016/j.autrev.2025.103823","url":null,"abstract":"<div><div>Autoimmune diseases (ADs) arise from the breakdown of immune tolerance to self-antigens, leading to pathological tissue damage. Proinflammatory cytokine overproduction disrupts redox homeostasis across diverse cell populations, generating oxidative stress that induces DNA damage through multiple mechanisms. Oxidative stress-induced alterations in membrane permeability and DNA damage can lead to the recognition of double-stranded DNA (dsDNA), mitochondrial DNA (mtDNA) and micronuclei-DNA (MN-DNA) by DNA sensors, thereby initiating activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. While previous reviews have characterized cGAS-STING activation in autoimmunity, the reciprocal regulation between redox homeostasis and cGAS-STING activation remains insufficiently defined. This narrative review examines oxidative stress-mediated DNA damage as a critical driver of pathological cGAS-STING signaling and delineates molecular mechanisms linking redox homeostasis to autoimmune pathogenesis. Furthermore, we propose therapeutic strategies that combine redox restoration with the attenuation of aberrant cGAS-STING activation, thereby establishing a mechanistic foundation for precision interventions in autoimmune disorders.</div></div><div><h3>Methods</h3><div>The manuscript is formatted as a narrative review. We conducted a comprehensive search strategy using electronic databases such as PubMed, Google Scholar and Web of Science. Various keywords were used, such as \"cGAS-STING,\" \"Redox homeostasis,\" \"Oxidative stress,\" \"pentose phosphate pathway,\" \"Ferroptosis,\" \"mtDNA,\" \"dsDNA,\" \"DNA damage,\" \"Micronuclei,\" \"Reactive oxygen species,\" \"Reactive nitrogen species,\" \"Nanomaterial,\" \"Autoimmune disease,\" \"Systemic lupus erythematosus,\" \"Type 1 diabetes,\" \"Rheumatoid arthritis,\" \"Multiple sclerosis,\" \"Experimental autoimmune encephalomyelitis,\" \"Psoriasis,\" etc. The titles and abstracts were reviewed for inclusion into this review. After removing duplicates and irrelevant studies, 174 articles met inclusion criteria (original research, English language).</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 6","pages":"Article 103823"},"PeriodicalIF":9.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143902534","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 double-negative B cells in the pathogenesis of systemic lupus erythematosus","authors":"Xinying Qiu ,&nbsp;RuiFan Wen ,&nbsp;Feifeng Wu ,&nbsp;Jueyi Mao ,&nbsp;Tasnim Azad ,&nbsp;Yang Wang ,&nbsp;Junquan Zhu ,&nbsp;Xin Zhou ,&nbsp;Haotian Xie ,&nbsp;Kimsor Hong ,&nbsp;Binbin Li ,&nbsp;Liang Zhang ,&nbsp;Chuan Wen","doi":"10.1016/j.autrev.2025.103821","DOIUrl":"10.1016/j.autrev.2025.103821","url":null,"abstract":"<div><div>B cells are essential to the pathophysiology of systemic lupus erythematosus (SLE), a chronic autoimmune illness. IgD-CD27-double negative B cells (DNB cells) are one of the aberrant B cell subsets linked to SLE that have attracted much scientific interest. There is growing evidence that DNB cells play a significant role in the development of the disease and are strongly linked to the activity of lupus. These cells play a pivotal role in the pathogenesis of SLE by producing a diverse array of autoantibodies, which form immune complexes that drive target organ damage. A comprehensive understanding of SLE pathophysiology necessitates in-depth investigation into DNB cells, not only to elucidate their mechanistic contributions but also to uncover novel therapeutic strategies.</div><div>According to available data, treatments that target B cells have proven effective in managing SLE; nevertheless, a significant breakthrough in precision medicine for SLE may come from targeting DNB cells specifically. Despite growing interest in DNB cells, their precise characteristics, developmental trajectories, and regulatory mechanisms remain incompletely defined, posing significant challenges to the field. A comprehensive investigation of the regulatory mechanisms governing DNB cell differentiation and expansion in SLE may facilitate novel therapeutic discoveries. This review aims to provide an updated synthesis of current research on DNB cells, with a focus on their origins, developmental trajectories in SLE, and potential as precision therapeutic targets.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103821"},"PeriodicalIF":9.2,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143876676","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 interleukin inhibitors in the treatment of hidradenitis suppurativa; a systematic review of clinical trials","authors":"Nazila Heidari ,&nbsp;Amirhossein Heidari ,&nbsp;Sara Eghbali ,&nbsp;Homayoun Pishraft-sabet ,&nbsp;Arman Hajikarim-Hamedani ,&nbsp;Yekta Ghane ,&nbsp;Zahra Lotfi ,&nbsp;Azadeh Goodarzi","doi":"10.1016/j.autrev.2025.103818","DOIUrl":"10.1016/j.autrev.2025.103818","url":null,"abstract":"<div><div>Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder that presents significant treatment challenges. Recent advancements have enhanced our understanding of its pathophysiology, leading to the development of novel therapeutic strategies. This systematic review evaluates the role of interleukin (IL) inhibitors as emerging treatment options for HS. A systematic search was conducted in PubMed/Medline, Scopus, and Web of Science databases for studies published up to September 2nd, 2024, with inclusion limited to clinical trials available in English. The National Institute of Health (NIH) Quality Assessment Tool for clinical trials and before-after studies with no control group was used to assess the methodological quality of the included studies. Out of 1289 studies, 20 met our inclusion criteria involving 3957 patients. Moreover, four ongoing trials were retrieved from ClinicalTrials.gov. Secukinumab showed sustained hidradenitis Suppurativa Clinical Response (HiSCR) improvements, particularly in biologic-naïve patients with common adverse events (AEs). Bimekizumab was effective with biweekly dosing, while the four-week regimen had inconsistent results, with rare reports of AEs. Brodalumab and bermekimab provided rapid and sustained HiSCR responses with lesion reductions, which were well tolerated. Guselkumab and ustekinumab showed promising but statistically nonsignificant improvements with mild AEs. Risankizumab did not significantly improve HiSCR rates but showed Dermatology Life Quality Index (DLQI) benefits. Anakinra offered moderate efficacy with prolonged exacerbation-free periods but led to some treatment discontinuations. Spesolimab reduced inflammatory lesions and draining tunnels while maintaining a favorable safety profile. IL inhibitors, especially IL-17 inhibitors, have demonstrated efficacy in treating moderate-to-severe HS, while IL-23 inhibitors have shown inconsistent results. Despite their generally favorable safety profiles, further research is needed to optimize treatment strategies and assess long-term outcomes.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103818"},"PeriodicalIF":9.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868284","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":"Macrophage polarization regulates the pathogenesis and progression of autoimmune diseases","authors":"Siwen Wu ,&nbsp;Shubi Zhao ,&nbsp;Lei Hai ,&nbsp;Ziyin Yang ,&nbsp;Shifen Wang ,&nbsp;Dawei Cui ,&nbsp;Jue Xie","doi":"10.1016/j.autrev.2025.103820","DOIUrl":"10.1016/j.autrev.2025.103820","url":null,"abstract":"<div><div>Macrophages are integral components of the innate immune system, present in nearly all tissues and organs throughout the body. They exhibit a high degree of plasticity and heterogeneity, participating in immune responses to maintain immune homeostasis. When the immune system loses tolerance, macrophages rapidly proliferate and polarize in response to various signaling pathways within a disrupted microenvironment. The direction of macrophage polarization can be regulated by a variety of factors, including transcription factors, non-coding RNAs, and metabolic reprogramming. Autoimmune diseases arise from the immune system's activation against host cells, with macrophage polarization playing a critical role in the pathogenesis of numerous chronic inflammatory and autoimmune conditions, such as rheumatoid arthritis, systemic lupus erythematosus, immune thrombocytopenic purpura, and type 1 diabetes. Consequently, elucidating the molecular mechanisms underlying macrophage development and function presents opportunities for the development of novel therapeutic targets. This review outlines the functions of macrophage polarization in prevalent autoimmune diseases and the underlying mechanisms involved. Furthermore, we discuss the immunotherapeutic potential of targeting macrophage polarization and highlight the characteristics and recent advancements of promising therapeutic targets. Our aim is to inspire further strategies to restore macrophage balance in preventing and treating autoimmune diseases.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103820"},"PeriodicalIF":9.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860079","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":"Janus kinase inhibitors for psoriatic arthritis: Evidence from a systematic review and network meta-analysis","authors":"Sotirios G. Tsiogkas ,&nbsp;Arriana Gkouvi ,&nbsp;Katerina Maria Kontouli ,&nbsp;Theodora Simopoulou ,&nbsp;Maria G. Grammatikopoulou ,&nbsp;Dimitrios P. Bogdanos","doi":"10.1016/j.autrev.2025.103819","DOIUrl":"10.1016/j.autrev.2025.103819","url":null,"abstract":"<div><div>Psoriatic arthritis (PsA) constitutes a heterogeneous disease. Diagnosis is commonly made by identifying joint inflammation, dactylitis, enthesitis, or axial spine involvement in cutaneous or nail psoriasis. Janus kinases (JAKs) are intracellular kinases that mediate cytokine signaling. The present network meta-analysis aimed to provide a comprehensive summary regarding the use of JAK inhibitors (JAKis) in PsA. We systematically searched MEDLINE, CENTRAL, Web of Science databases, and the <span><span>clinicaltrials.gov</span><svg><path></path></svg></span> registry until October 2023 and included randomized controlled trials (RCTs). Examined outcomes consisted of the proportion of participants achieving ACR20, ACR50, ACR70, PASI75, resolution of enthesitis, resolution of dactylitis, and experiencing serious adverse events (SAEs). Changes in the Health Assessment Questionnaire Disability Index (HAQ-DI) from the baseline were also recorded. The revised Cochrane Risk of Bias 2.0 tool determined the risk of bias. Networks were constructed, and random-effects frequentist analyses were employed utilizing the placebo arms from each study. Most JAKis were superior to placebo for all examined outcomes. Statistical advantages of one JAKi over another were recorded, and all concerned upadacitinib. However, the safety profile of upadacitinib did not differ significantly from that of other JAKis. Our network meta-analysis is the first to concentrate on comparable, current outcome data of JAKis in PsA on clinical efficacy. It reveals statistically significant variations in the advantages and disadvantages among JAKis in PsA, which require further meticulous assessment.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 6","pages":"Article 103819"},"PeriodicalIF":9.2,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881449","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":"Autophagy in myositis, a dysregulated pathway, and a target for therapy","authors":"A.S. Kamalanathan ,&nbsp;Vikas Agarwal ,&nbsp;Laura Talamini ,&nbsp;Sylviane Muller","doi":"10.1016/j.autrev.2025.103817","DOIUrl":"10.1016/j.autrev.2025.103817","url":null,"abstract":"<div><div>Corticosteroids and immunosuppressants are the mainstay of therapy for idiopathic inflammatory myopathies (IIMs). However, a significant therapeutic challenge extends beyond mitigating inflammation with these agents in achieving meaningful improvements in muscle strength and physical function, a goal that remains largely unmet. IIMs encompass a heterogeneous group of autoimmune disorders, including dermatomyositis, polymyositis, necrotizing autoimmune myopathy, inclusion body myositis, and others, characterized by chronic muscle inflammation, progressive weakness, and fatigue. The etiology of IIMs remains poorly understood, though potential contributors include environmental triggers (<em>e.g.</em>, infections, medications, or injury) and genetic predisposition. To advance the development of novel therapeutic strategies, it is critical to elucidate the dysfunctional molecular and cellular pathways underlying IIM pathogenesis. Among these, dysregulated autophagy pathways have emerged as a promising target for therapeutic intervention. Specifically, impairments in lysosomal autophagy and mitophagy have been implicated in IIMs, and modulating these processes through targeted regulatory mechanisms may offer therapeutic benefits. This review provides a comprehensive synthesis of clinical and biological features of IIMs, the current diagnostic approaches and emerging biomarkers, evaluates the utility of existing biomarkers, and examines the relevance of animal models in IIM research. Furthermore, we explore the role of autophagic dysregulation in disease pathogenesis and provide a critical appraisal of current treatment modalities. Finally, we highlight emerging therapeutic targets and regulatory molecules under investigation, with a particular focus on autophagy modulation. Notably, autophagy inhibitors represent a novel and potentially transformative therapeutic avenue for patients with IIMs, offering hope for improved clinical outcomes.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103817"},"PeriodicalIF":9.2,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143878335","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 entrenchment of NLRP3 inflammasomes in autoimmune disease-related inflammation","authors":"Valeria Carnazzo ,&nbsp;Donato Rigante ,&nbsp;Giuliana Restante ,&nbsp;Valerio Basile ,&nbsp;Krizia Pocino ,&nbsp;Umberto Basile","doi":"10.1016/j.autrev.2025.103815","DOIUrl":"10.1016/j.autrev.2025.103815","url":null,"abstract":"<div><div>Autoinflammation and autoimmunity are almost “opposite” phenomena characterized by chronic activation of the immune system, ‘innate’ in the first and ‘adaptive’ in the second, leading to inflammation of several tissues with specific protean effectors of tissue damage. The mechanism of involvement of multiprotein complexes called ‘inflammasomes’ within autoimmune pictures, differently from autoinflammatory conditions, is yet undeciphered. In this review we provide a comprehensive overview on NLRP3 inflammasome contribution into the pathogenesis of some autoimmune diseases. In response to autoantibodies against nucleic acids or tissue-specific antigens the NLRP3 inflammasome is activated within dendritic cells and macrophages of patients with systemic lupus erythematosus. Crucial is NLRP3 inflammasome to amplify tissue inflammation with interleukin-1 overexpression and matrix metalloproteinase production at the joint level in rheumatoid arthritis. A deregulated NLRP3 inflammasome activation occurs in the serous acini of salivary and lacrimal glands prone to Sjogren's syndrome, but also in the inflammatory process involving endothelial cells, leucocyte recruitment, and platelet plugging of vasculitides. Furthermore, organ-specific autoimmune diseases such as thyroiditis and hepatitis may display hyperactive NLRP3 inflammasomes at the level of resident immune cells within thyroid or liver, respectively. Therefore, it is not unexpected that preclinical studies have shown how specific inflammasome inhibitors may significantly overthrow the severity of different autoimmune diseases and slow down their trend towards an ominous progression. Specific markers of inflammasome activation could also reveal subclinical inflammatory components escaping conventional diagnostic approaches or improve monitoring of autoimmune diseases and personalizing their treatment.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 7","pages":"Article 103815"},"PeriodicalIF":9.2,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143833289","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}