First paragraph (this article has no abstract)

It has been well established that the pathogenesis of rheumatoid arthritis (RA) comprises three distinct but interdependent phenomena: the hyperplasia of synovial tissue, chronic inflammation (both local and systemic), and alterations in the immune response, including changes in the T-cell repertoire and the production of autoantibodies [1]. The precise nature of these interactions, however, particularly the role of autoantibodies in RA pathogenesis, is not yet fully understood. Whilst the occurrence of autoantibodies has been recognised as a characteristic feature of disease, and certain autoantibodies have become valuable tools for diagnosis, their contribution to the initiation and perpetuation of disease has remained largely elusive.