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Apoptosis in Rheumatoid Synoviocytes

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Rheumatoid arthritis (RA) is systemic autoimmune disease characterized by synovial proliferation and infiltration of various inflammatory cells. The process of disease progression, characterized by hyperplasia of synoviocytes, mainly of synovial fibroblasts, results in cartilage and bone destruction. Proliferation of synoviocytes is, however, not limitless, and spontaneous arrest and remission of synovial proliferation are occasionally observed. Previous studies from our laboratories as well as by other investigators have demonstrated that RA synoviocytes express functional Fas antigen (CD95/APO-1) and that these cells undergo Fas-mediated apoptosis both in vivo and in vitro. These findings suggest that Fas-mediated apoptosis may play a critical role in the regression of synovial hyperplasia in RA. Identification of regulatory mechanisms in RA synoviocytes may provide important insights and may lead us to establish novel strategies for RA therapy. We describe a current study by our laboratory on the regulatory mechanisms of apoptosis in RA, especially FasL and FADD gene transfer into inflamed synovium to induce remission stage and propose a novel strategy termed `apomodulation' in the treatment of RA.

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  • Rheumatoid Arthritis
  • Autoimmune Disease
  • Inflammatory Cell
  • Gene Transfer
  • Regulatory Mechanism