Pub Date : 2025-12-03DOI: 10.1038/s41584-025-01337-3
Rachel Knevel
Advances in artificial intelligence (AI) are transforming patient stratification in rheumatology. In 2025, three landmark studies demonstrated how multimodal AI approaches spanning clinical, molecular and longitudinal data can uncover distinct disease subtypes and predict therapeutic response, advancing the field towards precision rheumatology.
{"title":"Advances in AI-based patient stratification for rheumatic diseases","authors":"Rachel Knevel","doi":"10.1038/s41584-025-01337-3","DOIUrl":"10.1038/s41584-025-01337-3","url":null,"abstract":"Advances in artificial intelligence (AI) are transforming patient stratification in rheumatology. In 2025, three landmark studies demonstrated how multimodal AI approaches spanning clinical, molecular and longitudinal data can uncover distinct disease subtypes and predict therapeutic response, advancing the field towards precision rheumatology.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"75-77"},"PeriodicalIF":32.7,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664281","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 : 2025-12-03DOI: 10.1038/s41584-025-01332-8
Kelsey H. Collins, Ida K. Haugen, Tuhina Neogi, Farshid Guilak
Osteoarthritis (OA) is a painful disorder of the synovial joints characterized by dysfunctional cellular metabolism and extracellular matrix degradation that activates maladaptive repair responses, including pro-inflammatory pathways of innate immunity. OA has historically been viewed as an unavoidable consequence of ageing owing to wear-and-tear of the joint. Most strategies to mitigate OA have primarily focused on the articular cartilage and, more recently, other specific joint tissues, which limits understanding of OA as a systemic disease beyond the joint. Preclinical and clinical data support a paradigm shift in understanding OA as a disease of the whole person, focusing on changes throughout the body that both promote and are caused by OA. This shift provides novel insights into why preclinical research findings have not been successfully translated into clinical therapies. Moreover, a viable strategy for OA drug development could be to treat pain separately from OA structural damage. Challenging classically held views that lack evidence or have been disproven is required for progress. We explore some key emerging questions that should be carefully considered in future OA studies. Adapting and integrating new technologies, techniques, and tools into the rapidly evolving understanding of OA could lead to the development of drugs that might not only treat OA but also provide mechanistic insight into other conditions that result from the dysregulation of systemic factors or from the communication breakdown in inter-organ crosstalk. Such developments would reposition OA researchers from adapting approaches from other fields of science and medicine to leaders in the fight against chronic disease. Emerging evidence suggests a paradigm shift in viewing osteoarthritis (OA) as a systemic, bidirectional disease. This Review examines the current data supporting this concept, outlines key challenges in research approaches, and proposes strategies to improve preclinical studies and clinical trial design.
{"title":"Osteoarthritis as a systemic disease","authors":"Kelsey H. Collins, Ida K. Haugen, Tuhina Neogi, Farshid Guilak","doi":"10.1038/s41584-025-01332-8","DOIUrl":"10.1038/s41584-025-01332-8","url":null,"abstract":"Osteoarthritis (OA) is a painful disorder of the synovial joints characterized by dysfunctional cellular metabolism and extracellular matrix degradation that activates maladaptive repair responses, including pro-inflammatory pathways of innate immunity. OA has historically been viewed as an unavoidable consequence of ageing owing to wear-and-tear of the joint. Most strategies to mitigate OA have primarily focused on the articular cartilage and, more recently, other specific joint tissues, which limits understanding of OA as a systemic disease beyond the joint. Preclinical and clinical data support a paradigm shift in understanding OA as a disease of the whole person, focusing on changes throughout the body that both promote and are caused by OA. This shift provides novel insights into why preclinical research findings have not been successfully translated into clinical therapies. Moreover, a viable strategy for OA drug development could be to treat pain separately from OA structural damage. Challenging classically held views that lack evidence or have been disproven is required for progress. We explore some key emerging questions that should be carefully considered in future OA studies. Adapting and integrating new technologies, techniques, and tools into the rapidly evolving understanding of OA could lead to the development of drugs that might not only treat OA but also provide mechanistic insight into other conditions that result from the dysregulation of systemic factors or from the communication breakdown in inter-organ crosstalk. Such developments would reposition OA researchers from adapting approaches from other fields of science and medicine to leaders in the fight against chronic disease. Emerging evidence suggests a paradigm shift in viewing osteoarthritis (OA) as a systemic, bidirectional disease. This Review examines the current data supporting this concept, outlines key challenges in research approaches, and proposes strategies to improve preclinical studies and clinical trial design.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"105-117"},"PeriodicalIF":32.7,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145664532","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 : 2025-12-02DOI: 10.1038/s41584-025-01296-9
Juhi R. Kuchroo, Naomi Goldman, Arlene H. Sharpe
Immune-checkpoint molecules have essential roles in regulating immune responses, which maintain the delicate balance between physiological immune reactions and autoimmunity. The clinical success of immune checkpoint blockade for cancer therapy, and the occurrence of immune-related adverse events during cancer immunotherapy, highlight the profound effect of modulating these receptors on both tumour-specific and ‘self’-specific responses. As a result, interest in exploring how these molecules can be targeted to treat autoimmune and rheumatological diseases is expanding. Targeting of the immune-checkpoint molecules PD-1, B and T lymphocyte attenuator (BTLA) and T cell immunoreceptor with Ig and ITIM domains (TIGIT) to induce immune tolerance has shown therapeutic promise in pre-clinical models and, in some instances, clinical trials. A comprehensive understanding of how these receptors function in various immune cell populations, particularly T cells, and across different diseases is crucial for the successful translation of these findings to clinical applications. Immune-checkpoint agonists are a promising therapeutic approach for autoimmune disease. This Review discusses the immune-checkpoint receptors PD-1, BTLA and TIGIT as well as the preclinical and clinical evidence for therapeutically targeting these receptors for the treatment of rheumatic diseases.
{"title":"PD-1, BTLA and TIGIT as therapeutic targets for rheumatic disease","authors":"Juhi R. Kuchroo, Naomi Goldman, Arlene H. Sharpe","doi":"10.1038/s41584-025-01296-9","DOIUrl":"10.1038/s41584-025-01296-9","url":null,"abstract":"Immune-checkpoint molecules have essential roles in regulating immune responses, which maintain the delicate balance between physiological immune reactions and autoimmunity. The clinical success of immune checkpoint blockade for cancer therapy, and the occurrence of immune-related adverse events during cancer immunotherapy, highlight the profound effect of modulating these receptors on both tumour-specific and ‘self’-specific responses. As a result, interest in exploring how these molecules can be targeted to treat autoimmune and rheumatological diseases is expanding. Targeting of the immune-checkpoint molecules PD-1, B and T lymphocyte attenuator (BTLA) and T cell immunoreceptor with Ig and ITIM domains (TIGIT) to induce immune tolerance has shown therapeutic promise in pre-clinical models and, in some instances, clinical trials. A comprehensive understanding of how these receptors function in various immune cell populations, particularly T cells, and across different diseases is crucial for the successful translation of these findings to clinical applications. Immune-checkpoint agonists are a promising therapeutic approach for autoimmune disease. This Review discusses the immune-checkpoint receptors PD-1, BTLA and TIGIT as well as the preclinical and clinical evidence for therapeutically targeting these receptors for the treatment of rheumatic diseases.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"89-104"},"PeriodicalIF":32.7,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145656837","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 : 2025-12-01DOI: 10.1038/s41584-025-01339-1
Christine T. N. Pham, Farshid Guilak
Many of the current therapies for arthritis lack a targeted approach, limiting clinical benefits. Nanoparticle-based delivery systems have enabled more precise and efficient delivery of therapeutic agents, particularly nucleic acids. Studies in 2025 emphasize the promise of these strategies for the treatment of various forms of arthritis.
{"title":"Advances in RNA-based nanotherapies for arthritis","authors":"Christine T. N. Pham, Farshid Guilak","doi":"10.1038/s41584-025-01339-1","DOIUrl":"10.1038/s41584-025-01339-1","url":null,"abstract":"Many of the current therapies for arthritis lack a targeted approach, limiting clinical benefits. Nanoparticle-based delivery systems have enabled more precise and efficient delivery of therapeutic agents, particularly nucleic acids. Studies in 2025 emphasize the promise of these strategies for the treatment of various forms of arthritis.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"80-81"},"PeriodicalIF":32.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145645158","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 : 2025-11-28DOI: 10.1038/s41584-025-01338-2
Maria Papatriantafyllou
T helper 17 cells that lose IL-17 expression drive inflammation in a mouse model of chronic rheumatoid arthritis.
在慢性类风湿关节炎小鼠模型中，失去IL-17表达的T辅助17细胞驱动炎症。
{"title":"ExTH17 cells maintain chronic inflammation in RA","authors":"Maria Papatriantafyllou","doi":"10.1038/s41584-025-01338-2","DOIUrl":"10.1038/s41584-025-01338-2","url":null,"abstract":"T helper 17 cells that lose IL-17 expression drive inflammation in a mouse model of chronic rheumatoid arthritis.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"74-74"},"PeriodicalIF":32.7,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145611241","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 : 2025-11-27DOI: 10.1038/s41584-025-01329-3
Fabian Proft, Andre L. Ribeiro, Shikha Singla, Vinod Chandran, Wilson Liao, Christine Lindsay, Enrique R. Soriano, Tina Bhutani, Atul Deodhar, Kurt de Vlam, Lihi Eder, Mitsumasa Kishimoto, Ying Ying Leung, Ennio Lubrano, Dennis McGonagle, Denis Poddubnyy, Laura Savage, Filip Van den Bosch, Philip Mease
Despite advances in the treatment of psoriatic arthritis (PsA), a substantial proportion of patients continue to report persistent symptoms and impaired quality of life. However, terminology remains inconsistent for patients who fail to achieve disease control despite treatment, which limits research comparability and contributes to therapeutic inertia. To address this gap, a Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) task force developed consensus definitions for two distinct states: complex-to-manage PsA (C2M-PsA) and treatment-refractory PsA (TR-PsA). C2M-PsA is defined as a state of persistent symptoms despite treatment with at least one biologic or targeted synthetic DMARD (b/tsDMARD), extending beyond biological non-response to include factors such as comorbidities, overlapping conditions, psychosocial burden and treatment-related challenges (for example, non-adherence). TR-PsA, a more specific subset of C2M-PsA, is characterized by failure of at least three therapies with distinct mechanisms of action (including at least two biologic/targeted synthetic DMARDs), persistent symptoms considered problematic by both patient and clinician, and objective evidence of ongoing inflammation — after ruling out alternative explanations for treatment refractoriness. These consensus-derived GRAPPA definitions provide a shared framework to standardize terminology, support individualized care, and improve patient stratification in research and practice. Prospective validation across diverse settings and phenotypes is needed to confirm their reliability, responsiveness and clinical utility. In this Consensus Statement, a Group for Research and Assessment of Psoriasis and Psoriatic Arthritis task force presents consensus definitions for two distinct states, complex-to-manage PsA and treatment-refractory PsA, with the aim of standardizing terminology, improving patient stratification and guiding clinical decision-making and future research.
{"title":"Consensus definitions of complex-to-manage and treatment-refractory psoriatic arthritis: a GRAPPA initiative","authors":"Fabian Proft, Andre L. Ribeiro, Shikha Singla, Vinod Chandran, Wilson Liao, Christine Lindsay, Enrique R. Soriano, Tina Bhutani, Atul Deodhar, Kurt de Vlam, Lihi Eder, Mitsumasa Kishimoto, Ying Ying Leung, Ennio Lubrano, Dennis McGonagle, Denis Poddubnyy, Laura Savage, Filip Van den Bosch, Philip Mease","doi":"10.1038/s41584-025-01329-3","DOIUrl":"10.1038/s41584-025-01329-3","url":null,"abstract":"Despite advances in the treatment of psoriatic arthritis (PsA), a substantial proportion of patients continue to report persistent symptoms and impaired quality of life. However, terminology remains inconsistent for patients who fail to achieve disease control despite treatment, which limits research comparability and contributes to therapeutic inertia. To address this gap, a Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) task force developed consensus definitions for two distinct states: complex-to-manage PsA (C2M-PsA) and treatment-refractory PsA (TR-PsA). C2M-PsA is defined as a state of persistent symptoms despite treatment with at least one biologic or targeted synthetic DMARD (b/tsDMARD), extending beyond biological non-response to include factors such as comorbidities, overlapping conditions, psychosocial burden and treatment-related challenges (for example, non-adherence). TR-PsA, a more specific subset of C2M-PsA, is characterized by failure of at least three therapies with distinct mechanisms of action (including at least two biologic/targeted synthetic DMARDs), persistent symptoms considered problematic by both patient and clinician, and objective evidence of ongoing inflammation — after ruling out alternative explanations for treatment refractoriness. These consensus-derived GRAPPA definitions provide a shared framework to standardize terminology, support individualized care, and improve patient stratification in research and practice. Prospective validation across diverse settings and phenotypes is needed to confirm their reliability, responsiveness and clinical utility. In this Consensus Statement, a Group for Research and Assessment of Psoriasis and Psoriatic Arthritis task force presents consensus definitions for two distinct states, complex-to-manage PsA and treatment-refractory PsA, with the aim of standardizing terminology, improving patient stratification and guiding clinical decision-making and future research.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 2","pages":"132-144"},"PeriodicalIF":32.7,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41584-025-01329-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145608735","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 : 2025-11-26DOI: 10.1038/s41584-025-01328-4
Joshua Heerey, Joanne Kemp, Pim van Klij, Vasco Mascarenhas, Mark Scholes, Fleur Boel, Paul Dijkstra, Kay Crossley, Sita Bierma-Zeinstra, Rintje Agricola
Hip morphology has emerged as an important factor in the development of hip osteoarthritis (OA). Cam morphology is one of the most common hip morphologies, characterized by a bony prominence around the femoral head–neck junction of the hip that alters the normal shape of the femoral head. Cam morphology can contribute to intra-articular joint damage by generating abnormal contact stresses at this junction, initiating femoroacetabular impingement (FAI) syndrome and eventually leading to hip OA. Cam morphology is a causal risk factor for hip OA, but not everybody with this morphology will develop FAI syndrome or OA. The pathogenesis of hip disease is probably driven by the interplay between cam morphology, other coexisting hip morphologies (such as pincer morphology), femoral version, spinopelvic parameters and biomechanical and environmental factors. Early identification of FAI syndrome could enable timely, multidisciplinary intervention and offers the potential to modify the trajectory of disease. Cam morphology can develop during skeletal maturation, particularly in adolescents participating in high-joint-load physical activity, raising important questions about preventative approaches. Management of FAI syndrome includes both surgical and non-surgical approaches. Emerging insights into the pathogenesis and detection of cam morphology are paving the way for more targeted interventions and a deeper understanding of its role in FAI syndrome and hip OA development. Cam morphology can cause intra-articular joint damage and lead to femoroacetabular impingement syndrome and eventually hip osteoarthritis. This Review explores the development and effect of cam morphology on femoroacetabular impingement syndrome and hip osteoarthritis, discussing relevant terminology, diagnostic approaches, pathophysiological insights and management strategies.
{"title":"Cam morphology and the development of femoroacetabular impingement syndrome and hip osteoarthritis","authors":"Joshua Heerey, Joanne Kemp, Pim van Klij, Vasco Mascarenhas, Mark Scholes, Fleur Boel, Paul Dijkstra, Kay Crossley, Sita Bierma-Zeinstra, Rintje Agricola","doi":"10.1038/s41584-025-01328-4","DOIUrl":"10.1038/s41584-025-01328-4","url":null,"abstract":"Hip morphology has emerged as an important factor in the development of hip osteoarthritis (OA). Cam morphology is one of the most common hip morphologies, characterized by a bony prominence around the femoral head–neck junction of the hip that alters the normal shape of the femoral head. Cam morphology can contribute to intra-articular joint damage by generating abnormal contact stresses at this junction, initiating femoroacetabular impingement (FAI) syndrome and eventually leading to hip OA. Cam morphology is a causal risk factor for hip OA, but not everybody with this morphology will develop FAI syndrome or OA. The pathogenesis of hip disease is probably driven by the interplay between cam morphology, other coexisting hip morphologies (such as pincer morphology), femoral version, spinopelvic parameters and biomechanical and environmental factors. Early identification of FAI syndrome could enable timely, multidisciplinary intervention and offers the potential to modify the trajectory of disease. Cam morphology can develop during skeletal maturation, particularly in adolescents participating in high-joint-load physical activity, raising important questions about preventative approaches. Management of FAI syndrome includes both surgical and non-surgical approaches. Emerging insights into the pathogenesis and detection of cam morphology are paving the way for more targeted interventions and a deeper understanding of its role in FAI syndrome and hip OA development. Cam morphology can cause intra-articular joint damage and lead to femoroacetabular impingement syndrome and eventually hip osteoarthritis. This Review explores the development and effect of cam morphology on femoroacetabular impingement syndrome and hip osteoarthritis, discussing relevant terminology, diagnostic approaches, pathophysiological insights and management strategies.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 3","pages":"199-212"},"PeriodicalIF":32.7,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145599896","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":"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
Obesity constitutes a substantial burden in psoriatic disease that affects approximately half of patients. Importantly, increased adiposity and psoriatic disease are strongly linked, with obesity functioning as both a possible trigger and a disease modifier. Obesity predisposes individuals to develop psoriasis and is likely to drive, at least partially, the progression from psoriasis to psoriatic arthritis. For people with psoriasis or psoriatic arthritis, obesity is associated with lower rates of remission and poorer responses to treatment. Several mechanisms probably underlie this relationship, including systemic and local pro-inflammatory properties of adipose tissue, increased biomechanical stress on joints and entheses, gut dysbiosis and synergistic effects of osteoarthritis. Notably, weight loss can improve both psoriatic disease course and response to therapy; however, current approaches (such as dietary interventions or bariatric surgery) are difficult to implement. Glucagon-like peptide-1-based therapies are an effective strategy for weight loss in psoriatic disease and might even have additive disease-modifying effects to conventional immunomodulators. Although often overlooked, weight loss intervention and obesity management should be included as an integral part of psoriatic disease treatment algorithms. This Review explores the complex relationship between obesity and psoriatic disease. The authors highlight the underlying mechanisms that drive this association and propose a comprehensive approach to managing obesity in individuals with psoriatic disease to improve overall disease management and therapeutic response.
{"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":"10.1038/s41584-025-01326-6","url":null,"abstract":"Obesity constitutes a substantial burden in psoriatic disease that affects approximately half of patients. Importantly, increased adiposity and psoriatic disease are strongly linked, with obesity functioning as both a possible trigger and a disease modifier. Obesity predisposes individuals to develop psoriasis and is likely to drive, at least partially, the progression from psoriasis to psoriatic arthritis. For people with psoriasis or psoriatic arthritis, obesity is associated with lower rates of remission and poorer responses to treatment. Several mechanisms probably underlie this relationship, including systemic and local pro-inflammatory properties of adipose tissue, increased biomechanical stress on joints and entheses, gut dysbiosis and synergistic effects of osteoarthritis. Notably, weight loss can improve both psoriatic disease course and response to therapy; however, current approaches (such as dietary interventions or bariatric surgery) are difficult to implement. Glucagon-like peptide-1-based therapies are an effective strategy for weight loss in psoriatic disease and might even have additive disease-modifying effects to conventional immunomodulators. Although often overlooked, weight loss intervention and obesity management should be included as an integral part of psoriatic disease treatment algorithms. This Review explores the complex relationship between obesity and psoriatic disease. The authors highlight the underlying mechanisms that drive this association and propose a comprehensive approach to managing obesity in individuals with psoriatic disease to improve overall disease management and therapeutic response.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":"22 3","pages":"151-164"},"PeriodicalIF":32.7,"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}
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