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A detailed examination of skin cytology in cutaneous lupus erythematosus has identified cellular interactions and an inflammatory environment that exist prior to lesion formation.
New research has identified a novel, de novo mutation in the TLR7 gene that increases the affinity of TLR7 for guanosine, leading to TLR7 overactivation and child-onset systemic lupus erthematosus.
Results from the R4RA clinical trial indicate that gene signatures in pre-treatment biopsy-derived synovial tissue can predict the response to biologic DMARDs in patients with rheumatoid arthritis.
New research reveals that outcomes for patients with rheumatoid arthritis are affected less by pre-existing comorbid conditions than by socioeconomic factors. Future research should address the mechanisms of this relationship and develop holistic treatment approaches that reduce disparities attributed to socioeconomic status.
The new ACR guideline for the treatment of juvenile idiopathic arthritis provides an update on several important topics, including management of oligoarthritis, temporomandibular joint arthritis and systemic-onset arthritis. Overall, the new guideline reflects changes in practice, but also highlights a concerning lack of high-quality evidence.
In this Review, the authors discuss the latest insights into how autoantibodies and autoreactive B cells relate to the disease process in rheumatoid arthritis, from the development of pre-disease seropositivity to the onset of overt symptoms and the maintenance of disease chronicity.
In this Review, the authors discuss the characterization of distinct synovial tissue macrophage (STM) populations and their functions in the context of the healthy and arthritic joint. They also describe how distinct STMs are specified, how they respond to danger signals and the clinical implications of understanding STM heterogeneity.
In this Review, the authors discuss how the inflammatory, hypoxic environment of joints in rheumatoid arthritis affects metabolism in fibroblasts, endothelial cells and immune cells. Understanding the competing requirements of these cells can enable effective therapeutic targeting of synovial metabolism.
In this Review, the authors provide an overview of the mechanisms contributing to joint damage in rheumatoid arthritis, particularly the interactions among immune cells, fibroblasts and bone, and discuss how this knowledge could inform the development of novel therapies.
