Two of the key events in the pathogenesis of rheumatoid arthritis are the synovial cell proliferation and lymphocyte infiltration into the synovium. The resulting synovitis is longlasting and leads to destructive arthritis, which is a hallmark of rheumatoid arthritis. Accumulating evidence suggests that one of the key biochemical events in the altered cell function of RA is phosphorylation of the tyrosine residues of proteins. In this paper we review the cellular components participating in the chronic inflammation of RA joints. We present the results of analyzing tyrosine phosphorylated proteins of synovial cells from RA patients and discuss a possible pathogenic role of non-receptor tyrosine kinase in RA.
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