Arthritis & Rheumatology最新文献

{"title":"Journal Club","authors":"","doi":"10.1002/art.70288","DOIUrl":"https://doi.org/10.1002/art.70288","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70288","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Journal Club","authors":"","doi":"10.1002/art.70288","DOIUrl":"https://doi.org/10.1002/art.70288","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70288","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Connections","authors":"","doi":"10.1002/art.70289","DOIUrl":"https://doi.org/10.1002/art.70289","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70289","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complement Activation Linked to Type II Interferon Signaling in Still Disease.","authors":"Freya M C H Huijsmans, Tabea Thalheim, Alejandra Bodelón, Greta Rogani, Lyanne J P M Sijbers, Remco G A Erkens, Aafke de Ligt, Rianne Scholman, Aron Brinker, Gisella B Beretta, Nienke M Ter Haar, Thomas Vogl, Johannes Roth, Trang T Duong, Sytze de Roock, Joost F Swart, Deborah A Marshall, Susanne M Benseler, Rae S M Yeung, Christoph Kessel, Sebastiaan J Vastert, Emely L Verweyen, Jorg van Loosdregt","doi":"10.1002/art.70307","DOIUrl":"10.1002/art.70307","url":null,"abstract":"<p><strong>Objective: </strong>Still disease (SD) is an autoinflammatory syndrome characterized by innate immune dysregulation. Although complement can drive inflammation, its involvement in SD remains to be defined. Thus, we aimed to assess complement activation in SD.</p><p><strong>Methods: </strong>Complement was assessed using transcriptomic, proteomic, and in vitro approaches. RNA sequencing of monocytes was performed in healthy donors (n = 15), those with nonsystemic juvenile idiopathic arthritis (JIA; n = 8), patients with SD at onset (n = 19) and remission (n = 18), and those with macrophage activation syndrome (n = 2). Whole-blood NanoString analysis of complement and interferon (IFN)-related gene expression was conducted in patients with SD (active n = 41, inactive n = 33) and JIA (n > 600). Complement products and inflammatory mediators were measured by Luminex and enzyme-linked immunosorbent assay. Functional complement activity was evaluated in SD (active n = 30, inactive n = 67) and JIA sera (n = 12). In vitro assays examined monocytic C1q induction and complement-mediated CD8⁺ T cell activation.</p><p><strong>Results: </strong>Transcriptomic analysis of monocytes from patients with SD at onset revealed enrichment of the complement cascade compared with patients in remission (adjusted P = 3.7 × 10^-36), ranking among the top 10 up-regulated pathways. Classical complement genes (C1QB/C1QC) were markedly up-regulated in onset SD compared with patients with remission SD and JIA. Patients with active SD showed increased C1q, C3a, C5a, and terminal complement complex protein levels, with enhanced functional classical complement activity. Whole-blood C1QB/C1QC expression correlated with IFN-related markers, including interleukin-18, CXCL9, and CXCL10. Recombinant IFN-γ induced monocytic C1q, whereas C1q enhanced IFN-γ production by CD8⁺ T cells, supporting a feed-forward loop.</p><p><strong>Conclusion: </strong>SD is characterized by complement activation with marked up-regulation of C1q, which is closely linked to IFN-γ/type II signaling.</p>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811586","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":"TWEAK/Fn14 Signaling Drives Oxidative Cardiac Injury in Systemic Lupus Erythematosus: Evidence From Patient Biomarker Studies, Lupus Mouse Models, and Cardiomyocyte Assays","authors":"Yale Liu MD, PhD,&nbsp;Zhu Yan MD,&nbsp;Xueting Peng MD,&nbsp;Meixuan Li MD,&nbsp;Juan Wang MD, PhD,&nbsp;Yan Zhang PhD,&nbsp;Xiaoqian Hu MD,&nbsp;Mingzhu Zhou MD,&nbsp;Kaixuan Ren MD,&nbsp;Dan Zhang PhD,&nbsp;Xingyi Guo PhD,&nbsp;Yumin Xia MD, PhD,&nbsp;Huanhuan Huo MD","doi":"10.1002/art.70110","DOIUrl":"10.1002/art.70110","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Cardiac involvement is a major cause of morbidity in systemic lupus erythematosus (SLE). Tumor necrosis factor–like weak inducer of apoptosis (TWEAK) is elevated in SLE, but its contribution to lupus-associated cardiac injury is unclear. We investigated the role of TWEAK/fibroblast growth factor–inducible 14 (Fn14) signaling in SLE-related cardiomyopathy and its potential as a biomarker and therapeutic target.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Serum TWEAK, inflammatory cytokines, autoantibodies, and oxidative stress markers were measured in 242 patients with SLE and 66 age- and sex-matched controls, with correlation to echocardiographic, electrocardiographic, and myocardial enzyme findings. Cardiac pathology and redox signaling were assessed in pristane-induced lupus models using wild-type mice and mice deficient of <i>Fn14</i> by histopathology, immunoblotting, immunofluorescence, and quantitative proteomics. Direct effects of TWEAK on mitochondrial oxidative stress, antioxidant signaling, and apoptosis were examined in primary cardiomyocytes isolated from MRL/lpr mice who were lupus prone.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Serum TWEAK levels were significantly elevated in patients with SLE and were highest in those with cardiac abnormalities compared with healthy controls. TWEAK correlated positively with malondialdehyde, 8-hydroxy-2’-deoxyguanosine, disease activity, and inflammatory cytokines and inversely with superoxide dismutase. Elevated baseline TWEAK predicted new cardiac abnormalities during follow-up and declined with clinical improvement. In mice with lupus, <i>Fn14</i> deficiency reduced cardiac reactive oxygen species accumulation, restored Nrf2/HO-1 antioxidant signaling, attenuated histopathological injury, and preserved cardiac function. In vitro, TWEAK induced mitochondrial superoxide production, suppressed Nrf2 signaling, and promoted apoptosis in lupus-prone cardiomyocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>TWEAK/Fn14 signaling drives oxidative stress–mediated cardiomyocyte injury in SLE and represents a promising biomarker and therapeutic target for lupus-associated cardiac damage.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1892-1906"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147288802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long Noncoding RNA H19 Mediates STAT3-Dependent Activation of Keratinocytes and Fibroblasts in Systemic Sclerosis Skin","authors":"Begoña Caballero-Ruiz PhD,&nbsp;Christopher W. Wasson PhD,&nbsp;Rebecca L. Ross PhD,&nbsp;Francesco Del Galdo MD","doi":"10.1002/art.70104","DOIUrl":"10.1002/art.70104","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Dermal systemic sclerosis (SSc) fibroblasts and their exosomes can activate keratinocytes in SSc, with long noncoding RNA (lncRNA) <i>H19</i> highlighted as the most up-regulated RNA in their cargo compared with healthy controls (HCs). The role of <i>H19</i> in SSc pathogenesis has never been investigated. Here we determine <i>H19</i>'s role in the profibrotic activation of dermal fibroblasts and in their crosstalk with keratinocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Skin biopsies were obtained from the forearms of patients with diffuse SSc (n = 20) or HCs (n = 8), and dermal fibroblasts were explanted. In situ hybridization was used to determine <i>H19</i> expression in the skin, paired with immunohistochemistry of STAT3 and Collagen1. <i>H19</i> and STAT3 expression were modulated by retroviral transduction and small interfering RNA. Gel contraction and Transwell coculture were employed for functional studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In SSc, high <i>H19</i> expression in skin and explanted dermal fibroblasts compared with HCs showed moderate correlation to well-described profibrotic markers. Knockdown of <i>H19</i> in SSc fibroblasts decreased profibrotic gene expression and cell contraction ability. <i>H19</i> overexpression was sufficient to induce a profibrotic phenotype in HC fibroblasts. Mechanistically, transforming growth factor-β, interleukin-6, and interleukin-11 significantly increased <i>H19</i> expression in HC fibroblasts (2.2-, 1.4-, and 3.5-fold, respectively) through activation of STAT3. Additionally, the STAT3 and STAT1 activation of keratinocytes induced by coculture with SSc fibroblasts was suppressed by <i>H19</i> knockdown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study shows that lncRNA <i>H19</i> is a key mediator of STAT3-induced changes in fibrotic activation of fibroblast and keratinocytes in SSc skin and could be considered a promising therapeutic target in tissue fibrosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1929-1941"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue-Specific and Spatially Dependent Metabolic Signatures Perturbed by Injury in Male and Female Mice","authors":"Hope D. Welhaven PhD,&nbsp;Avery H. Welfley BS,&nbsp;Priyanka P. Brahmachary PhD,&nbsp;Mark Greenwood PhD,&nbsp;Donald F. Smith PhD,&nbsp;Brian Bothner PhD,&nbsp;Ronald K. June PhD","doi":"10.1002/art.70098","DOIUrl":"10.1002/art.70098","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Osteoarthritis, the leading cause of disability worldwide, disproportionately affects women, yet sex remains an overlooked determinant. This disparity stems from sex-specific differences in injury susceptibility—a major risk factor for disease. Using a non-invasive injury model, we demonstrate that injury drives local and systemic metabolic alterations and that these responses differ by sex.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Male and female mice were subjected to non-invasive joint injury. Eight days after injury, serum, synovial fluid, and whole joints were collected for metabolomics. Additionally, whole joints were harvested for matrix-assisted laser desorption ionization–mass spectrometry imaging (MALDI-MSI) to capture the spatial distribution of molecular species and identify osteochondral regions perturbed by injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Comparative analyses among injured, contralateral, and naive mice revealed metabolomic alterations across sample types. Data indicate that injury influences metabolic profiles in whole joints, synovial fluid, and serum, with consistent dysregulation of amino acid, purine, and pyrimidine metabolism, indicating a systemic effect of localized injury. Additionally, sex-dependent differences emerged across tissues, highlighting sexually dimorphic pathways following injury. MALDI-MSI generated 2D ion images of bone, the joint interface, and bone marrow, identifying region-specific metabolic changes following injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Joint injury induces coordinated metabolic responses locally and systemically that extend beyond the injured joint and are influenced by sex. Integrating metabolomic and spatial analyses reveals how injury modulates joint pathophysiology across tissues and reveals sex-specific patterns relevant to post-traumatic osteoarthritis (PTOA) risk. These findings improve preclinical PTOA models and deepen our understanding of the complex role of injury and sex in osteoarthritis pathogenesis, laying the foundation for targeted therapeutic strategies.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1850-1862"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Role of Type I Interferon Signaling on Muscle Disease Using Mouse Models","authors":"Rita Spathis MS,&nbsp;Sabrina Narvesen BS,&nbsp;Deeva Robles Kuriplach BS,&nbsp;Karen Huang BS,&nbsp;Teja Sundar MS,&nbsp;Elizabeth Bagley BS,&nbsp;Joanna Parkes PhD,&nbsp;Xinyu Jia PharmD,&nbsp;Nandhana Sudhan,&nbsp;Alfredo Guzman MA,&nbsp;Kanneboyina Nagaraju PhD, DVM,&nbsp;Melissa Morales PhD","doi":"10.1002/art.70096","DOIUrl":"10.1002/art.70096","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Dysregulated type I interferon (IFN) signaling contributes to autoimmune myositis pathogenesis. We investigated the therapeutic effects of JAK inhibitors in two mouse models. We also examined how type I IFNs affect muscle vasculature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Myositis was induced in major histocompatibility complex class I double transgenic ([TRE-H-2K^b (H mice)/MCK-tTA (T mice)] (HT)) female mice at day 21. Mice were randomized into four groups (n = 10–11/group): baricitinib (10 mg/kg), tofacitinib (20 mg/kg), vehicle, and healthy controls. Outcomes included survival, weight, muscle strength, histopathology, and IFN-stimulated gene expression. To model IFNβ overexpression, C57BL/6 mice received AAV9-triple muscle-specific creatine kinase (tMCK)-IFNβ and were treated with vehicle or tofacitinib (40 mg/kg/day) for 10 weeks (n = 8–13/group).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Tofacitinib—but not baricitinib—significantly reduced IFN scores in mice with severe myositis (<i>P</i> &lt; 0.05). Survival differed across groups (overall log-rank <i>P</i> &lt; 0.01), with untreated- and baricitinib-treated HT mice showing shorter survival than BL/6 controls, whereas tofacitinib-treated mice did not differ from controls. IFNβ overexpression induced muscle inflammation (<i>P</i> &lt; 0.01), reduced grip strength (<i>P</i> &lt; 0.0001), and increased the IFN score (<i>P</i> &lt; 0.0001) and H2Kb (<i>P</i> &lt; 0.0001) expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Tofacitinib reduced the IFN signature, and survival in this group did not differ significantly from healthy controls, whereas untreated and baricitinib-treated HT mice showed shorter survival; functional improvement was not observed. Our results also show that type I IFN signaling contributes to muscle inflammation and weakness, making it a key driver of muscle damage and thereby reinforcing its potential as a therapeutic target.</p>\u0000 \u0000 <div>\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1942-1951"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/art.70096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omic Profiling Reveals Immune Cell Priming Signature Linked to Lupus Prognosis","authors":"Michael A. Smith PhD,&nbsp;Dominic Sinibaldi PhD,&nbsp;Saifur Rahman PhD, MBA,&nbsp;Chia-Chien Chiang PhD,&nbsp;Anna M. Hansen PhD,&nbsp;Jill Henault PhD,&nbsp;Carlos P. Roca PhD,&nbsp;Shu Wang BS,&nbsp;Kamelia Zerrouki MS,&nbsp;Rebecca Filippi MS,&nbsp;Christopher Groves BA,&nbsp;Zerai Manna MS,&nbsp;Jun Chu MSN, CRNP,&nbsp;Michael Davis MSN, CRNP,&nbsp;Sarthak Gupta MD,&nbsp;Christopher Morehouse MS,&nbsp;Melissa de los Reyes MS,&nbsp;Rachel Ettinger PhD,&nbsp;Roland Kolbeck PhD,&nbsp;Mariana J. Kaplan MD,&nbsp;Miguel A. Sanjuan PhD,&nbsp;Richard M. Siegel MD, PhD,&nbsp;Sarfaraz A. Hasni MD, MSc,&nbsp;Kerry A. Casey PhD","doi":"10.1002/art.70105","DOIUrl":"10.1002/art.70105","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Systemic lupus erythematosus (SLE) is a multiorgan disease with widespread immune dysregulation and significant unmet clinical need. Blood-based gene expression studies have advanced our understanding of SLE pathogenesis but may overlook critical tissue-specific mechanisms that drive disease heterogeneity and progression. We posited that integrated multidimensional profiling could reveal novel molecular patterns underlying distinct SLE pathologies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Here, we integrated immune cell, protein, and transcriptome data sets with disease activity and damage indices across 87 patients with SLE to reveal three independent protein signatures corresponding to discrete organ pathologies and immune perturbations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Alongside type I interferon and granulocyte pathways, our multidimensional analyses identified a previously uncharacterized immune cell priming protein signature that was enriched in patients with renal involvement and was indicative of elevated risk of six-year organ damage accrual. This minimally invasive signature outperformed conventional assessments and was only found in the serum proteomics data. Collectively, the protein signatures demonstrated a combined prevalence of 94%, reflecting their broad relevance to SLE.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Together, these results reveal parallel immune mechanisms in SLE and provide a framework to identify new therapeutic targets. Clinical and immune data are available for public exploration through the interactive SLE Immune Atlas.</p>\u0000 </section>\u0000 </div>","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1878-1891"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Genome-Wide Association Study Signal to Mechanism in Rheumatoid Arthritis: Lessons From a Single Risk Locus","authors":"Ryuya Edahiro MD, PhD,&nbsp;Yukinori Okada MD, PhD","doi":"10.1002/art.70182","DOIUrl":"10.1002/art.70182","url":null,"abstract":"","PeriodicalId":129,"journal":{"name":"Arthritis & Rheumatology","volume":"78 9","pages":"1819-1822"},"PeriodicalIF":9.9,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694966","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}