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The release of TGFβ by a subset of ITGA5+ synovial fibroblasts can promote the differentiation of pathogenic PD-1hiCXCL13+ T cells in RA, altering the inflammatory niche.
New research suggests that insulin-like growth factor 1 is an important contributor to Wnt-induced joint damage, and that its suppression could represent a promising therapeutic strategy for osteoarthritis.
A study reports that adipocytes can regulate the metabolism of fibroblasts in the healthy synovium via cortisol, but in inflammatory arthritis adiposity is lost and fibroblasts become pathogenic.
New classification criteria for axial disease in juvenile spondyloarthritis aim to enhance the identification and study of this condition in affected youth, offering a tool for future non-interventional studies and interventional trials. Better understanding of the efficacy of various interventions in the axial domain could help tailor treatment strategies.
EULAR and the Paediatric Rheumatology European Society (PReS) now view systemic juvenile idiopathic arthritis and adult-onset Still’s disease as a single disease — Still’s disease — given their overlapping biomarkers, clinical manifestations and complications. This consensus provides valuable insights into Still’s disease diagnosis and management across age groups, and also highlights research priorities.
The identification of shared molecular mechanisms across systemic inflammatory autoimmune diseases with overlapping clinical manifestations has prompted research into the underlying genetics that could be driving these manifestations; elucidating these genes could aid in the diagnosis, treatment and outcome prediction of these complex diseases.
In this Review, Nigrovic and colleagues examine potential mechanisms underlying the paradoxical continuation of inflammation in arthritis, despite the increased numbers of regulatory T cells in inflamed joints, and discuss the implications for regulatory T cell-targeted therapeutic interventions in inflammatory arthritis.
This Review provides a comprehensive update on dysregulated type I interferon production and signalling in autoinflammatory interferonopathies, monogenic systemic lupus erythematosus and conditions that present with broad immune dysregulation and interferon signatures. The authors provide a classification for autoinflammatory interferonopathies based on disease mechanisms of increased type I interferon production and signalling and overlapping clinical phenotypes.
This Review provides an update on autoantibodies associated with idiopathic inflammatory myopathies in both adults and children. The authors also discuss methods of autoantibody detection and the advantages and limitations of each technique.
