RA (rheumatoid arthritis) is a chronic rheumatic condition hallmarked by joint inflammation and destruction by self-reactive immune responses. Clinical management of RA patients is often hampered by its heterogeneous nature in both clinical presentation and outcome, thereby highlighting the need for new predictive biomarkers. In this sense, several studies have recently revealed a role for type I IFNs (interferons), mainly IFNα, in the pathogenesis of a subset of RA patients. Genetic variants associated with the type I IFN pathway have been linked with RA development, as well as with clinical features. Moreover, a role for IFNα as a trigger for RA development has also been described. Additionally, a type I IFN signature has been associated with the early diagnosis of RA and clinical outcome prediction in patients undergoing biological drug treatment, two challenging issues for decision-making in the clinical setting. Moreover, these cytokines have been related to endothelial damage and vascular repair failure in different autoimmune disorders. Therefore, together with chronic inflammation and disease features, they could probably account for the increased cardiovascular disease morbidity and mortality of these patients. The main aim of the present review is to provide recent evidence supporting a role for type I IFNs in the immunopathology of RA, as well as to analyse their possible role as biomarkers for disease management.

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