T cell-independent joint destruction

Rheumatoid Arthritis (RA) is a chronic systemic disorder of unknown etiology. Although, early and late stages of the disease may be driven by different processes, affected joints are characterized by inflammation, synovial hyperplasia, and abnormal immune responses [1]. The abundance of T cells within the rheumatoid synovium as well as the association of certain major histocompatibility complex (MHC) class II molecules with RA [2] implied a central role for T cells in the pathophysiology of the disease. However, recent advances in molecular biology have fostered new concepts for the pathogenesis of RA. Specifically, the investigation of early stages of disease, the development of novel anim…