Abstract
The rheumatic diseases are a diverse group of conditions that can display autoantibody production, functional immune disturbances and systemic disease manifestations. These autoantibodies can serve as markers for classification, diagnosis, prognosis and disease activity. Among specificities prominently expressed by patients, those directed to nuclear antigens (antinuclear antibodies or ANAs) are markers for specific rheumatic diseases. ANAs can bind to DNA, RNA and complexes of proteins with nucleic acids. Other autoantibodies expressed in the rheumatic diseases are directed to proteins, including IgG, post-translational modifications of proteins and soluble mediators such as cytokines. While autoantibodies have been investigated for over 50 years, recent studies published in the Annals of the Rheumatic Diseases (ARD) have provided an exciting perspective on the mechanisms of autoantibody production and the power of new technologies to identify novel autoantibody targets to elucidate aetiology and underpin patient evaluation. Furthermore, in-depth serological studies have demonstrated a phenomenon known as clustering; clustering defines sets of autoantibodies that are commonly expressed together in patients with a given rheumatic disease. Other research reported in ARD has used B cell phenotyping and genotypic analysis to subtype patients, and has explored the relationship of autoantibodies, complement activation and patterns of gene expression as exemplified by the interferon gene signature. Together, these studies provide important new insights into disease mechanisms as well as actionable information to facilitate personalised patient care.