ABSTRACT
Rheumatoid arthritis (RA) is characterized by the intense infiltration of activated T lymphocytes into the synovium. These activated T cells are to play an instrumental role in the initiation and perpetuation of chronic rheumatoid synovitis (1-3). Although the traditional use of slow-acting antirheumatic drugs (SAARDS) intends to down-regulate the chronic inflammatory response within the synovium, such agents are limited by their incomplete, unpredictable, and poorly sustained clinical benefits (4,5). Moreover, these agents are largely nonspecific in their alteration of effector immune responses (4). For these reasons alternative therapies have emerged to selectively interfere with leukocyte number and function. Therapies such as thoracic duct drainage, total lymphoid irradiation, leukapheresis, and cyclosporine have been studied because of their ability to abrogate circulating T-cell/leukocyte number or activity (6). Unfortunately, the clinical utility of such therapies has been hampered by the limited clinical responses and/or unacceptable toxicities. Newer approaches to therapy in RA have largely focused on the quantitative or qualitative impairment of T-cell function with the hope of achieving greater disease control.
