The role of immunologic processes in the pathogenesis of rheumatoid arthritis (RA) is indisputable. Histopathologic and ultrastructural studies of rheumatoid synovium show synovial lining cell hyperplasia, along with subintimal chronic inflammatory cell infiltrates that include T cells, B cells. and macrophages. Rheumatoid factor, anti-collagen and other locally produced antibodies, and a number of soluble mediators that contribute to joint destruction, such as prostaglandins and collagenase, are produced in large amounts by synovial tissue cells. In most models of RA synovitis it is theorized that T cells orchestrate the local inflammatory response. In these paradigms, an arthrotropic agent, such as a virus or bacterial cell wall fragments, or an “autoantigen,” such as type I1 collagen, proteoglycan, or Ia molecules, serves as a stimulus for T cell activation. The antigen-specific T cells preferentially expand in the synovium and recruit and/or influence other cells (including macrophages, B cells, and fibroblasts) through the elaboration of lymphokines. Al-though this might be true in the initial phases of RA, the evidence of T cell primacy in established, chronic synovitis is not definitive.