ABSTRACT
Rheumatoid arthritis (RA) is characterized by chronic inflammation in multiple joints and concomitant destruction of cartilage and bone. Macrophages play a crucial role in both the inflammatory process and tissue destruction.1-3
Macrophages become activated by the RA process in the synovial tissue, either directly through stimulation with bacterial or viral triggers, or indirectly through T-and B-cell-mediated events. The latter responses can be directed to joint-specific autoantigens, but may also include reactions to persistent viral and bacterial elements. Although RA has been considered an autoimmune process, a crucial autoantigen has not been defined and it seems more likely that multiple candidate triggers are involved. This argues for general therapeutic approaches at a downstream level, making activated macrophages an obvious target.
