ABSTRACT
Rheumatoid arthritis (RA) is an immunologically mediated, chronic inflammatory disease characterized by synovial cell proliferation, inflammation, and destruction of adjacent mticular tissue (I). Although considerable evidence supports the importance of immune processes in the pathogenesis of RA ( l the underlying cause is unknown. The prevailing view is that RA is mediated by antigenactivated T cells that infiltrate the synovial membrane and initiate a series of inflammatory processes, resulting in vascular and synovial cell proliferation with resorption of cartilage and bone (3). Nonimmunologica! pathways also probably contribute to tissue injury and destruction in established RA (4). Degradation of articular extracellular matrix components is a hallmark of RA and is largely mediated by neutral proteinases such as collagenase, stromelysin, elastase, and cathepsin G. A schematic diagram of cellular and humoral pathways implicated in the pathogenesis of RA is presented in Figure l. The model suggests several opportunities for interruption of these pathways that could be exploited in treating autoimmune disorders such as RA.
