{"title":"Positive phase II trial of IL-17A–IL-17F-targeting nanobody sonelokimab for PsA","authors":"Holly Webster","doi":"10.1038/s41584-025-01335-5","DOIUrl":"10.1038/s41584-025-01335-5","url":null,"abstract":"A nanobody that targets IL-17A and IL-17F has shown promise in a phase II study of patients with active psoriatic arthritis.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"4-4"},"PeriodicalIF":32.7,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145599341","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}
Pub Date : 2025-11-24DOI: 10.1038/s41584-025-01326-6
Rebecca H. Haberman, Alexis Ogdie, Joseph F. Merola, Jose U. Scher, Lihi Eder
{"title":"The obesity–inflammation axis in psoriatic disease: mechanisms and therapeutic strategies","authors":"Rebecca H. Haberman, Alexis Ogdie, Joseph F. Merola, Jose U. Scher, Lihi Eder","doi":"10.1038/s41584-025-01326-6","DOIUrl":"https://doi.org/10.1038/s41584-025-01326-6","url":null,"abstract":"","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"100 1","pages":""},"PeriodicalIF":33.7,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145583189","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}
Pub Date : 2025-11-24DOI: 10.1038/s41584-025-01334-6
Sarah Onuora
The results of the phase II DAHLIAS trial support the development of the neonatal Fc receptor blocker nipocalimab for the treatment of Sjögren disease.
{"title":"Nipocalimab reduces Sjögren disease activity in phase II trial","authors":"Sarah Onuora","doi":"10.1038/s41584-025-01334-6","DOIUrl":"10.1038/s41584-025-01334-6","url":null,"abstract":"The results of the phase II DAHLIAS trial support the development of the neonatal Fc receptor blocker nipocalimab for the treatment of Sjögren disease.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"4-4"},"PeriodicalIF":32.7,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145593739","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}
Pub Date : 2025-11-19DOI: 10.1038/s41584-025-01321-x
George A. Robinson, Andrea Knight, Lori B. Tucker, Alexandre Belot, David A. Isenberg, Coziana Ciurtin
Childhood-onset systemic lupus erythematosus (SLE) is associated with more active disease trajectories, increased cardiovascular risk, earlier development of organ damage (which commonly affects the kidney, central nervous and musculoskeletal systems) and increased use of glucocorticoids and immunosuppressive treatments than adult-onset SLE. However, the understanding of immunopathogenic mechanisms in childhood-onset SLE is far less established than in adult-onset disease. Technological advances over the past decade have accelerated progress in understanding the immune, genetic, epigenetic, metabolic and proteomic profiles of childhood-onset SLE, and have also established the mechanistic roles of immune dysregulation, interferon signalling, biological sex, gender and ethnicity in shaping disease heterogeneity. These insights have led to the elucidation of the mechanisms that drive the increased severity of childhood-onset SLE and point towards new pathways for personalized therapeutic approaches aimed at improving long-term outcomes and quality of life for patients. Childhood-onset SLE is characterized by high disease activity, severe organ damage and substantial treatment challenges. The authors of this Review provide an update on the advances in the understanding of the pathogenesis of childhood-onset SLE in the past decade, emphasizing the need for more research to improve outcomes.
{"title":"Insights into the pathogenesis of childhood-onset SLE in the past decade","authors":"George A. Robinson, Andrea Knight, Lori B. Tucker, Alexandre Belot, David A. Isenberg, Coziana Ciurtin","doi":"10.1038/s41584-025-01321-x","DOIUrl":"10.1038/s41584-025-01321-x","url":null,"abstract":"Childhood-onset systemic lupus erythematosus (SLE) is associated with more active disease trajectories, increased cardiovascular risk, earlier development of organ damage (which commonly affects the kidney, central nervous and musculoskeletal systems) and increased use of glucocorticoids and immunosuppressive treatments than adult-onset SLE. However, the understanding of immunopathogenic mechanisms in childhood-onset SLE is far less established than in adult-onset disease. Technological advances over the past decade have accelerated progress in understanding the immune, genetic, epigenetic, metabolic and proteomic profiles of childhood-onset SLE, and have also established the mechanistic roles of immune dysregulation, interferon signalling, biological sex, gender and ethnicity in shaping disease heterogeneity. These insights have led to the elucidation of the mechanisms that drive the increased severity of childhood-onset SLE and point towards new pathways for personalized therapeutic approaches aimed at improving long-term outcomes and quality of life for patients. Childhood-onset SLE is characterized by high disease activity, severe organ damage and substantial treatment challenges. The authors of this Review provide an update on the advances in the understanding of the pathogenesis of childhood-onset SLE in the past decade, emphasizing the need for more research to improve outcomes.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"26-41"},"PeriodicalIF":32.7,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145545246","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}
Pub Date : 2025-11-18DOI: 10.1038/s41584-025-01330-w
Holly Webster
Findings reveal that inhibiting cytosolic phospholipase A2 in chondrocytes could be a potential therapeutic target for degenerative joint diseases.
研究结果表明，抑制软骨细胞的胞质磷脂酶A2可能是退行性关节疾病的潜在治疗靶点。
{"title":"cPLA2 as a therapeutic target in chondrocytes for OA and IVDD","authors":"Holly Webster","doi":"10.1038/s41584-025-01330-w","DOIUrl":"10.1038/s41584-025-01330-w","url":null,"abstract":"Findings reveal that inhibiting cytosolic phospholipase A2 in chondrocytes could be a potential therapeutic target for degenerative joint diseases.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"3-3"},"PeriodicalIF":32.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145536431","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}
Pub Date : 2025-11-17DOI: 10.1038/s41584-025-01331-9
Mandana Nikpour, Kathleen Morrisroe, Alicia Calderone, Deborah Yates, Alan Silman
{"title":"Author Correction: Occupational dust and chemical exposures and the development of autoimmune rheumatic diseases","authors":"Mandana Nikpour, Kathleen Morrisroe, Alicia Calderone, Deborah Yates, Alan Silman","doi":"10.1038/s41584-025-01331-9","DOIUrl":"10.1038/s41584-025-01331-9","url":null,"abstract":"","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"71-71"},"PeriodicalIF":32.7,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41584-025-01331-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531674","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}
Pub Date : 2025-11-13DOI: 10.1038/s41584-025-01323-9
Martina Rauner, Aline Bozec
Rheumatoid arthritis is an autoimmune disease that affects ~1% of the global population and leads to joint inflammation, local bone erosions and systemic bone loss. The disability and immobility caused by inflammatory bone loss, joint destruction and fractures in rheumatoid arthritis present a clinical challenge and impose a considerable socioeconomical burden. Osteoclasts have the unique ability to resorb bone and cause bone loss. A comprehensive understanding of the regulatory mechanisms of osteoclasts and their crosstalk with stromal cells, such as osteoblasts, or immune cells during inflammation is essential for the development of targeted therapies to prevent and treat bone loss. The objective of this Review is to present a comprehensive overview of the current knowledge of osteoclast regulation at different levels: from systemic pathways to changes in the bone microenvironment, including the involvement of local cells, to osteoclast-intrinsic regulation such as metabolic adaptations. We also discuss some of the current and emerging therapies that can counteract inflammatory bone loss. The factors and mechanisms that regulate osteoclast-induced inflammatory bone loss are complex. The authors of this Review provide an overview of osteoclast regulation in the context of inflammatory bone loss and rheumatoid arthritis and provide insights into potential treatment strategies.
{"title":"Mechanisms of osteoclast activation in inflammatory bone loss in rheumatoid arthritis","authors":"Martina Rauner, Aline Bozec","doi":"10.1038/s41584-025-01323-9","DOIUrl":"10.1038/s41584-025-01323-9","url":null,"abstract":"Rheumatoid arthritis is an autoimmune disease that affects ~1% of the global population and leads to joint inflammation, local bone erosions and systemic bone loss. The disability and immobility caused by inflammatory bone loss, joint destruction and fractures in rheumatoid arthritis present a clinical challenge and impose a considerable socioeconomical burden. Osteoclasts have the unique ability to resorb bone and cause bone loss. A comprehensive understanding of the regulatory mechanisms of osteoclasts and their crosstalk with stromal cells, such as osteoblasts, or immune cells during inflammation is essential for the development of targeted therapies to prevent and treat bone loss. The objective of this Review is to present a comprehensive overview of the current knowledge of osteoclast regulation at different levels: from systemic pathways to changes in the bone microenvironment, including the involvement of local cells, to osteoclast-intrinsic regulation such as metabolic adaptations. We also discuss some of the current and emerging therapies that can counteract inflammatory bone loss. The factors and mechanisms that regulate osteoclast-induced inflammatory bone loss are complex. The authors of this Review provide an overview of osteoclast regulation in the context of inflammatory bone loss and rheumatoid arthritis and provide insights into potential treatment strategies.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"42-61"},"PeriodicalIF":32.7,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498235","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}
Pub Date : 2025-11-07DOI: 10.1038/s41584-025-01322-w
Lam C. Tsoi, John Varga
Circulating cell-free DNA (cfDNA) and cfDNA fragmentation signatures are emerging as promising non-invasive biomarkers for various indications, most notably cancer. New analysis of cfDNA fragmentation in autoimmunity highlights potential links to cancer, as well as the promise of these tools for improved understanding and clinical care of autoimmune disease.
{"title":"Cell-free DNA fragmentation signatures link cancer and autoimmunity","authors":"Lam C. Tsoi, John Varga","doi":"10.1038/s41584-025-01322-w","DOIUrl":"10.1038/s41584-025-01322-w","url":null,"abstract":"Circulating cell-free DNA (cfDNA) and cfDNA fragmentation signatures are emerging as promising non-invasive biomarkers for various indications, most notably cancer. New analysis of cfDNA fragmentation in autoimmunity highlights potential links to cancer, as well as the promise of these tools for improved understanding and clinical care of autoimmune disease.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 1","pages":"6-7"},"PeriodicalIF":32.7,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145461820","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}
Pub Date : 2025-11-07DOI: 10.1038/s41584-025-01325-7
Jessica McHugh
A new population-based study suggests that sodium–glucose cotransporter-2 (SGLT2) inhibitors — originally developed for glycaemic control — reduce the risk of autoimmune rheumatic diseases.
{"title":"SGLT2 inhibitors reduce risk of autoimmune disease","authors":"Jessica McHugh","doi":"10.1038/s41584-025-01325-7","DOIUrl":"10.1038/s41584-025-01325-7","url":null,"abstract":"A new population-based study suggests that sodium–glucose cotransporter-2 (SGLT2) inhibitors — originally developed for glycaemic control — reduce the risk of autoimmune rheumatic diseases.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"21 12","pages":"698-698"},"PeriodicalIF":32.7,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455474","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}
Pub Date : 2025-11-07DOI: 10.1038/s41584-025-01318-6
Benjamin Klein, Allison C. Billi, Lisa Abernathy-Close, J. Michelle Kahlenberg
Cutaneous lupus erythematosus (CLE) is a complex inflammatory skin disease that presents either in isolation or as a frequent manifestation of systemic lupus erythematosus (SLE). CLE subtypes show clinical heterogeneity and varying associations with SLE. Histologically, CLE is characterized by interface dermatitis, a reaction pattern that involves immune-cell infiltration of the dermo-epidermal junction. In-depth characterization of both non-lesional and lesional lupus skin has reshaped our understanding of pathogenesis. Non-lesional and lesional lupus skin exhibits early and chronic upregulation of type I interferons, which drive photosensitivity, myeloid-cell recruitment and amplification of cytokine responses in both immune and non-immune cells. This detailed understanding of CLE biology has enabled the development of targeted therapies. Ongoing research to identify key pathogenic mechanisms will create opportunities for prevention of CLE and CLE-to-SLE transition. This Review discusses latest advances in the field of cutaneous lupus, including the improved understanding of disease pathogenesis and emerging targeted therapies.
{"title":"Cutaneous lupus erythematosus — from pathogenesis to targeted therapy","authors":"Benjamin Klein, Allison C. Billi, Lisa Abernathy-Close, J. Michelle Kahlenberg","doi":"10.1038/s41584-025-01318-6","DOIUrl":"10.1038/s41584-025-01318-6","url":null,"abstract":"Cutaneous lupus erythematosus (CLE) is a complex inflammatory skin disease that presents either in isolation or as a frequent manifestation of systemic lupus erythematosus (SLE). CLE subtypes show clinical heterogeneity and varying associations with SLE. Histologically, CLE is characterized by interface dermatitis, a reaction pattern that involves immune-cell infiltration of the dermo-epidermal junction. In-depth characterization of both non-lesional and lesional lupus skin has reshaped our understanding of pathogenesis. Non-lesional and lesional lupus skin exhibits early and chronic upregulation of type I interferons, which drive photosensitivity, myeloid-cell recruitment and amplification of cytokine responses in both immune and non-immune cells. This detailed understanding of CLE biology has enabled the development of targeted therapies. Ongoing research to identify key pathogenic mechanisms will create opportunities for prevention of CLE and CLE-to-SLE transition. This Review discusses latest advances in the field of cutaneous lupus, including the improved understanding of disease pathogenesis and emerging targeted therapies.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"21 12","pages":"703-718"},"PeriodicalIF":32.7,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455476","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}
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