Pathogenesis of rheumatoid arthritis: The role of synoviocytes

Rheumatoid arthritis (RA) is traditionally considered to be a T-cell-mediated disease. Additional data have implicated T-cell-independent pathways in its pathogenesis, however, especially in late stages of the disease.(26, 32) No one can reasonably dispute that RA is a disease involving immunologic processes(34,84) ; however, the specific contribution of T cells as initiators or perpetuators of the disease remains difficult to prove. Non-T-cell elements, including macrophage and fibroblast-like synoviocytes (FLS), are capable of producing cytokines and matrix-degrading enzymes in the joint, proliferating, and invading adjacent tissues, perhaps in an autonomous fashion. These non-T-cell participants could play an essential role in destructive aspects of the disease. In this article, we mainly focus on FLS among these constituents of RA synovial tissues and discuss the characteristics of these cells in relation to transformation, signal transduction, and production of enzymes responsible for joint destruction.