Autoimmunity reviews最新文献

{"title":"Mitochondria-melanosome crosstalk in pigmentary disorders: Implications for alopecia areata pathogenesis.","authors":"Xu Liu, Sheng Wan, Shiqi Fu, Xiaoxia Sheng, Xiuzu Song","doi":"10.1016/j.autrev.2026.104204","DOIUrl":"https://doi.org/10.1016/j.autrev.2026.104204","url":null,"abstract":"<p><p>Organellar communication between mitochondria and melanosomes serves as a cornerstone of pigment cell biology, orchestrating bioenergetics, ion dynamics, and organelle remodeling during melanogenesis. Recent mechanistic insights reveal that melanosomal STIM1 engages mitochondrial Mitofusin-2 (Mfn2) upon calcium depletion to channel localized ATP for V-type ATPase-driven acidification, enabling PMEL amyloidogenesis. Concurrently, mitochondrial fission factor (MFF) translocates to melanosomes to assemble an ARP2/3-dependent actin network required for organelle scission and structural integrity. In Alopecia Areata (AA)-an autoimmune disorder classically characterized by hair follicle immune privilege collapse-active bulb melanocytes represent a primary vulnerable locus, as illustrated by clinical hallmarks such as the selective loss of pigmented hair (\"canities sparing\") and initial white hair regrowth (poliosis). Here, we synthesize how environmental or genetic stressors destabilize this mitochondria-melanosome axis: mitochondrial Ca²⁺ overload and respiratory uncoupling dismantle STIM1-Mfn2 tethers and disrupt MFF scission, resulting in bioenergetic crisis, \"aborted\" melanization, and melanosomal membrane peroxidation. The ensuing release of damage-associated molecular patterns (DAMPs) and carbonylated neoantigens activates the NLRP3 inflammasome and cGAS-STING pathway, driving ectopic MHC class I expression and recruiting autoreactive CD8⁺ T cells to execute targeted follicular destruction. By critically stratifying histopathologically proven AA endpoints from extrapolated vitiligo and epidermal melanocyte data, this review reframes AA within an organelle-centric pathogenic paradigm and highlights emerging therapeutic interventions targeting the mitochondria-melanosome axis.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104204"},"PeriodicalIF":9.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223153","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":"Genetic and non-genetic drivers of immune dysregulation: Beyond autoinflammation and autoimmunity.","authors":"Yvan Jamilloux, Clarisse Doutriaux, Maurane Lepage, Nora Martel, Thomas Henry","doi":"10.1016/j.autrev.2026.104202","DOIUrl":"https://doi.org/10.1016/j.autrev.2026.104202","url":null,"abstract":"<p><p>Immune dysregulation spans a continuum from autoinflammation to autoimmunity and primary immune disorders, and arises from the interplay between genetic lesions and multiple layers of biological regulation. Monogenic diseases have provided critical models to dissect this complexity, yet phenotype is not determined by DNA sequence alone. The same gene can give rise to distinct clinical entities depending on variant functional class, position within functional domains, residual activity, isoform usage and cell- or tissue-specific effects, while carriers of identical variants may have variable phenotype due to somatic mosaicism, clonal dynamics, allelic expression bias, modifier genetics or environmental buffering. This review examines the major determinants of penetrance and variable expressivity across mechanistically informative immune disorders. We first analyze variant-intrinsic mechanisms using archetypal genes including MEFV, NLRP3, PLCG2 and UBA1, highlighting how distinct functional classes reshape disease identity. We then discuss how cellular context, somatic variation, allelic expression and X-linked regulation modify effective gene dosage in vivo. We further integrate multilocus inheritance, common and rare modifiers, interferonopathies, monogenic lupus-like diseases and primary immune disorders characterized by blended autoimmunity, autoinflammation and host-defense defects. Finally, we examine epigenetic, environmental and life-course drivers and their implications for diagnosis, counseling and precision therapy. Together, these data support a model in which genotype defines a framework rather than a fixed outcome. A mechanism-based view of immune dysregulation is therefore required to move from genetic diagnosis to meaningful prediction of disease expression and therapeutic response.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104202"},"PeriodicalIF":9.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223148","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":"Torque teno virus monitoring for precision immunosuppression in systemic autoimmune diseases.","authors":"Marc Scherlinger","doi":"10.1016/j.autrev.2026.104197","DOIUrl":"https://doi.org/10.1016/j.autrev.2026.104197","url":null,"abstract":"<p><p>Systemic autoimmune diseases often require long-term immunosuppression to control disease activity and prevent organ damage. However, immunosuppressive drugs increase the risk of infections, which remain among the leading causes of hospitalization and premature mortality in these conditions. The persistent therapeutic dilemma between too low and too severe immunosuppression is a major challenge in rheumatology practice, and very few tools exist to evaluate and follow the degree of immunosuppression in patients with systemic autoimmune diseases. Torque teno virus (TTV) is a non-pathogenic single-stranded DNA virus, which infects virtually everybody. TTV has emerged as a candidate biomarker of the net state of immunosuppression. TTV replication is dynamically constrained by host immune surveillance; blood viral load rises when immune control is impaired and falls when immune competence is restored. In solid organ transplantation, high TTV loads have been associated with infectious complications, whereas low loads have been associated with graft rejection, supporting the concept that TTV reports the balance between over- and under-immunosuppression. This Review summarizes the biological rationale for TTV monitoring, critically appraises transplantation evidence, reviews emerging data in systemic autoimmune disease, and proposes a translational framework for TTV-guided precision immunomodulation in systemic autoimmune diseases to be evaluated in future studies.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104197"},"PeriodicalIF":9.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178589","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":"Asia induced by hyaluronic acid, tattoos, hyaluronidase and polypropylene mesh.","authors":"Olga Vera-Lastra, Javier Juárez Medrano, Brayan Assael Carrasco Pérez, Elsa Acosta Jimenez, Abihai Lucas Hernández, Ana Lilia Peralta Amaro, Gabriela Medina, María Del Pilar Cruz Domínguez, Jesús Sepúlveda Delgado, Yehuda Shoenfeld","doi":"10.1016/j.autrev.2026.104194","DOIUrl":"https://doi.org/10.1016/j.autrev.2026.104194","url":null,"abstract":"<p><p>The growing use of cosmetic fillers, tattoos, and surgical meshes has brought increasing attention to their potential inflammatory and immunologic complications. Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) proposes a framework for systemic manifestations reported after exposure to these materials in susceptible individuals. Although hyaluronic acid is a natural component of the extracellular matrix with low immunogenicity and high biocompatibility, Hyaluronic acid fillers (HAF) have been associated with delayed inflammatory and granulomatous foreign-body reactions, and ASIA. Treatment includes corticosteroids and immunosuppressive (IS) agents and hyaluronidase which dissolves injected HAF, but it can cause allergic reactions. Tattoo pigments may provide a persistent immunological stimulus. Proposed mechanisms include cytokine-mediated immune activation, oxidative stress, and the release of nuclear antigens that may promote autoantibody production. Reported manifestations range from local inflammatory reactions to uveitis, sarcoidosis, and systemic autoimmune conditions. Treatment includes corticoids, IS, pigment removal and Lasser may be considered in selected cases. Similarly, Polypropylene Mesh (PPM) used in hernia and pelvic organ prolapse repair induces a persistent foreign-body response. Selected clinical reports describe ASIA-like manifestations after implantation, but population-based studies have not demonstrated an increased risk of defined systemic autoimmune disease. Across these exposures, delayed symptom onset, nonspecific manifestations, and the absence of a specific biomarker complicate diagnosis and causal attribution. Early recognition requires careful assessment of exposure history, local and systemic findings, and alternative diagnoses. Distinguishing established local complications from suspected systemic ASIA is essential to guide individualized treatment, while further controlled studies are needed to clarify causality and therapeutic outcomes.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104194"},"PeriodicalIF":9.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164824","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":"A temporal framework of redox dysregulation in autoimmunity: interplay between oxidative deficiency and oxidative stress.","authors":"Stefan Kim, Katelyn Kim, Shilpi Singh, Gatikrushna Singh","doi":"10.1016/j.autrev.2026.104193","DOIUrl":"10.1016/j.autrev.2026.104193","url":null,"abstract":"<p><p>Reactive oxygen species (ROS) occupy a paradoxical position in autoimmune disease: excessive or dysregulated ROS contribute to oxidative injury and inflammatory amplification, whereas physiological ROS function as spatially and temporally regulated signals required for immune homeostasis. This duality suggests that redox dysregulation may involve not only excessive ROS but also failure of physiologically required ROS signaling. We define this latter state as oxidative deficiency: a functionally defined state in which an inadequate physiological ROS signal impairs a specific redox-dependent biological process, rather than simply reflecting low total ROS or increased antioxidant capacity. Genetic and experimental studies of NADPH oxidase (NOX) pathways demonstrate that impaired NOX-dependent ROS generation can modify immune regulation and autoimmune susceptibility in selected contexts, with particularly strong support in systemic lupus erythematosus and experimental arthritis. However, divergent findings in experimental autoimmune encephalomyelitis and protection from autoimmune diabetes following reduced NOX2 activity demonstrate substantial disease- and function-specific effects. We therefore propose that oxidative deficiency and pathological oxidative stress represent distinct, independently testable dimensions of autoimmune-associated redox dysregulation whose relationship may be sequential, concurrent, or absent depending on disease context. In selected settings, oxidative deficiency may precede and later coexist with pathological oxidative stress, although direct temporal evidence for this trajectory in human autoimmune disease remains limited. The framework is experimentally falsifiable: evidence for oxidative deficiency requires demonstration of an inadequate physiological ROS signal, impairment of the corresponding biological function, and, where feasible, functional rescue following selective restoration of the deficient signal. This framework extends established redox concepts by distinguishing failure of physiological ROS signaling from pathological oxidant excess and provides testable criteria for defining their roles in autoimmune disease.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104193"},"PeriodicalIF":9.8,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164919","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":"Elderly-onset rheumatoid arthritis versus polymyalgia rheumatica: A systematic review and meta-analysis on pathophysiology, diagnosis and clinical progression.","authors":"Elvis Hysa, Emanuele Gotelli, Rosanna Campitiello, Stefano Soldano, Carmen Pizzorni, Sabrina Paolino, Vanessa Smith, Alberto Sulli, Maurizio Cutolo","doi":"10.1016/j.autrev.2026.104196","DOIUrl":"10.1016/j.autrev.2026.104196","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Elderly-onset rheumatoid arthritis (EORA) and polymyalgia rheumatica (PMR) are among the most frequent inflammatory rheumatic diseases in patients over 50, yet their clinical differentiation, particularly when EORA presents with polymyalgic onset, poses a common diagnostic challenge. This systematic review aimed to identify the pathophysiological, clinical, imaging and treatment-response features that distinguish EORA from PMR. MEDLINE, CENTRAL and Scopus (inception to January 2026), with supplementary searches of LILACS, Google Scholar and trial registries (June 2026) were searched, including studies that compared EORA with PMR or reported separately extractable data for both; risk of bias was appraised with design-specific tools and the evidence weighted accordingly. Seventy-one studies across four domains were included: pathophysiology (22 studies), clinical presentation and final diagnosis at follow-up (24 studies), imaging (21 studies), and treatment response (4 studies). Genetically, in one low risk of bias study that stratified EORA by rheumatoid factor status, PMR and seronegative EORA shared HLA-DRB1*13/*14 associations, a pattern distinct from the shared epitope-driven susceptibility of seropositive RA. However, divergent metabolomic signatures suggest different downstream inflammatory mechanisms. An exploratory random-effects meta-analysis yielded a pooled PMR-to-RA reclassification rate of 7% (95% CI 4-12%; 9 studies), narrowing to 4% (95% CI 2-7%) in methodologically robust studies, though rates of reclassification to RA were considerably higher (up to 20%) when patients with undifferentiated polymyalgic presentations were included. Peripheral arthritis occurred in 28% of PMR patients (95% CI 20-35%; 6 studies), with a significant difference between baseline prevalence (21%) and cumulative incidence over follow-up (34%) on subgroup meta-analysis (p = 0.026), and was characteristically transient and glucocorticoid-responsive, whereas persistent synovitis involving wrists and small joints was associated with reclassification to RA. On imaging, evidence from low-to-moderate risk of bias, ultrasound studies showed that shoulder findings overlapped substantially between conditions, whereas bilateral hip synovitis was significantly more frequent in PMR (47% vs 0% in RA), suggesting the hip as a stronger proximal informative site. However, distal joint synovitis demonstrated the highest discriminatory value, with the presence of at least one among RF positivity, hand grey-scale ≥2, or hand power Doppler ≥1 achieving 89% sensitivity and 93% specificity for EORA identification. This review highlights that the distinction between EORA and PMR cannot be reliably established at a single time point and that longitudinal reassessment integrating clinical, serological, and imaging findings remains essential for the differential diagnosis. However, the evidence is limited by clinical and methodological heterogeneity and the predominance of obs","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104196"},"PeriodicalIF":9.8,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164062","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":"Functional characterization of genetic variants associated with response to tumor necrosis factor inhibitors in psoriatic arthritis patients.","authors":"Angeliki Planaki, Theodora Simopoulou, Themistoklis Giannoulis, Efterpi Zafiriou, Dimitrios P Bogdanos, Theologia Sarafidou, Kalliopi Liadaki","doi":"10.1016/j.autrev.2026.104195","DOIUrl":"10.1016/j.autrev.2026.104195","url":null,"abstract":"<p><p>Psoriatic arthritis is a chronic, progressive inflammatory disease associated with psoriasis, affecting joints, entheses, and the axial skeleton. Treatment options have evolved from broad immunosuppressive therapies to targeted biologic agents. These therapies are generally safe and effective, but patient response varies considerably, emphasizing the importance of pharmacogenetic studies in the identification of variants that predict treatment response. This review explores the potential functional significance and causality of variants that were associated with response to tumor necrosis factor inhibitors by assessing their regulatory impact on gene expression, alternative splicing, transcription factor binding, chromatin state, and chromatin accessibility, using a combination of in silico resources. This integrated analysis revealed novel regulatory roles for specific variants. The variants rs1801274 in FCGR2A and rs396991 in FCGR3A have established biological roles in inflammation. The risk allele of variant rs767455 in TNFRSF1A correlates with increased TNFRSF1A expression and favors the splicing event that generates a TNFRSF1A soluble isoform lacking exon 6, resulting in increased inflammation. The variant rs20575 within TNFRSF10A correlates with the expression of the nearby inflammatory TNFRSF10D gene. The TNF variant rs1800610 correlates with changes in the expression of many nearby genes of the Human Leukocyte Antigen region. The variant rs610604, located within TNFAIP3, correlates with changes in the expression and splicing isoforms of WAKMAR2, a lncRNA with an anti-inflammatory role. In conclusion, the majority of variants associated with treatment response show strong evidence of a potential role in inflammation and psoriatic arthritis and may serve as clinical biomarkers pending replication and functional validation.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104195"},"PeriodicalIF":9.8,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164430","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 and systemic sclerosis: Mechanistic insights and microbial therapies.","authors":"Qi Liu, Yulin Wang, Mengmeng Pei, Ruihua Li, Rui Gao, Mingjie Gao, Min Chen, Yufang Gong, Ming Li, Biao Ni","doi":"10.1016/j.autrev.2026.104192","DOIUrl":"10.1016/j.autrev.2026.104192","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is an autoimmune disease characterized by progressive fibrosis in the skin and multiple organs. The cause and mechanism of SSc remain largely elusive, and there are limited therapeutic options available that effectively alter the progression of fibrosis associated with the disease. Emerging evidence indicates that the gut microbiota and its metabolites play a crucial regulatory role in maintaining immune homeostasis and modulating fibrotic responses in SSc. In this review, we provide a comprehensive summary of clinical evidence regarding gut microbiota dysbiosis in SSc, examines the potential mechanisms of gut microbiota involvement in SSc pathogenesis, and discusses recent advancements in diagnostic and therapeutic approaches based on gut microbiota for SSc. Finally, we emphasize the current limitations as well as future research directions. We aim to comprehensively present the current status of research on the relationship between gut microbiota and SSc, thereby offering valuable insights for further exploration of the pathogenesis of the disease and the development of personalized therapeutic strategies based on the gut microbiota and its metabolites.</p>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":" ","pages":"104192"},"PeriodicalIF":9.8,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103505","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":"IgA vasculitis sibling clustering: From HLA-DRB1 genetic burden to nephritis risk stratification","authors":"Lingjia Ren ,&nbsp;Xu Yan ,&nbsp;Xia Zhang ,&nbsp;Xu Jixiang ,&nbsp;Miao Jiang ,&nbsp;Xianqing Ren ,&nbsp;Ying Ding","doi":"10.1016/j.autrev.2026.104110","DOIUrl":"10.1016/j.autrev.2026.104110","url":null,"abstract":"<div><div>IgA vasculitis (IgAV) is the most common systemic small-vessel vasculitis in childhood, with an annual incidence of 3 to 26.7 per 100,000 children. Although it is predominantly sporadic, its 1.9% familial clustering rate and significant tendency for sibling comorbidity suggest a non-random pathogenesis. Multicohort GWAS data confirm that HLA-DRB1*01 and HLA-DRB1*11 are common genetic risk loci across ethnic groups. Furthermore, the core pathogenic molecule, galactose-deficient IgA1 (Gd-IgA1), exhibits a heritability of up to 64% in affected families, constituting the intrinsic basis for sibling concordance. Regarding the triggering mechanism, approximately 75% of IgAV cases are preceded by upper respiratory or gastrointestinal prodromal infections; the cross-transmission of streptococci and viruses within the family environment provides the external trigger for sibling-to-sibling transmission. Clinical phenotypes show that familial cases exhibit high consistency in the pattern of target organ involvement, and the renal involvement in the index case has significant predictive value for stratifying sibling risk. This article proposes potential mechanisms underlying the synchronized onset of disease and the formation of phenotypic mirroring among siblings, aiming to establish a clinical system for early warning and precise intervention based on family history.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 8","pages":"Article 104110"},"PeriodicalIF":8.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142547","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":"Comment on “Meta-analysis of meteorological conditions and rheumatoid arthritis”","authors":"Feng Luo ,&nbsp;Xueming Yao ,&nbsp;Wukai Ma","doi":"10.1016/j.autrev.2026.104006","DOIUrl":"10.1016/j.autrev.2026.104006","url":null,"abstract":"<div><div>This correspondence addresses critical methodological limitations in the recent meta analysis by Hu et al. regarding meteorological conditions and rheumatoid arthritis (RA). We highlight issues of clinical heterogeneity arising from the conflation of disparate outcomes and inconsistent follow-up durations. Furthermore, we identify a “quality score paradox” where small-sample studies are disproportionately rated as high-quality compared to large-scale evidence. Finally, we argue that pooling data across incompatible climatic zones neglects the effect of baseline adaptation, and we suggest that the observed association between atmospheric pressure and joint swelling supports a hydraulic physical mechanism distinct from immune-mediated inflammatory flares.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"25 3","pages":"Article 104006"},"PeriodicalIF":8.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146193936","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}