Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
As the pace of genetic discovery has accelerated, so too has the need for clinicians and researchers to acknowledge and understand the impact of language in scientific publications. The use of inaccurate language contributes to systemic bias and eugenic ideologies that remain pervasive in biomedical science, including in rheumatology.
Type 2 innate lymphoid cells protect against kidney inflammation in lupus nephritis, and enhancing their adhesion via integrin α4β7 upregulation, particularly through IL-33 treatment, could be a promising therapeutic approach.
Treatment with the endogenous metabolite itaconate induced phenotypic and metabolic changes in fibroblast-like synoviocytes and reduced the severity of arthritis in an animal model.
The management of antiphospholipid syndrome is hindered by heterogeneous clinical presentations. Whole-blood transcriptomics have the potential to identify previously unknown disease endotypes, which could inform new treatment strategies. However, such hypothesis-generating data must still account for the results of randomized clinical trials, such as those focused on direct oral anticoagulants in APS.
This Review outlines the role of platelets in Kawasaki disease and the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and highlights therapeutic strategies that target platelets or platelet-derived molecules.
Sjögren syndrome is a chronic autoimmune disease affecting exocrine glands, causing dryness and systemic symptoms. Treatment has been primarily symptomatic, but advances in our understanding of its pathophysiology offer promise for targeted therapies, aiming for personalized care and improved outcomes.
Integrins are involved in joint tissue development and homeostasis, and perturbations in the availability of integrin ligands or in downstream integrin signalling are linked to the pathogenesis of osteoarthritis (OA). This Review discusses current evidence and future perspectives for therapeutically targeting integrins in OA.
Genetic, epigenetic and transcriptomic studies in hyperuricaemia and gout have, in the past 6 years, provided important insights into the underlying molecular mechanisms, revealing new inflammatory pathways and epigenetic factors and expanding research beyond European populations.