Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease leading to inevitable joint destruction. An increased proliferation and hyperplasia of synovial lining cells in synovial tissue of affected joint is observed. Moreover, production of pro-inflammatory cytokines, chemokines, and accumulation of immunocompetent cells within the joint is also observed. Current research is specifically focused on the concept of synovial fibroblasts in the pathogenesis of RA. These cells are activated by pro-inflammatory cytokines secreted by macrophages and leukocytes, thereafter responding by an increased production of matrix degrading enzymes that lead to progressive joint destruction. RA synovial fibroblasts have also invasive potential independently on the presence of both immunocompetent cells and pro-inflammatory cytokines. In this overview, the author discusses morphology of synovial fibroblasts, altered apoptosis, and interaction of fibroblasts with immunocompetents cells. Furthermore, cytokine-independent activation of synovial fibroblasts, and the role of activated fibroblasts in the process of joint destruction within the pathogenesis of RA are also mentioned.

        Key words: rheumatoid arthritis, pro-inflammatory cytokines, synovial fibroblasts