Direct interaction of immunoglobulins with synovial fibroblasts: a missing link in the pathogenesis of rheumatoid arthritis?

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.