Multiple cytokines play a pivotal role in the pathogenesis of rheumatoid arthritis (RA). For this to happen, the appropriate intracellular signaling pathways must be activated via cytokine receptors on the cell surface. Among them, members of JAK family are essential for the signaling pathways of various cytokines and are implicated in the pathogenesis of RA. An orally available JAK3 inhibitor tofacitinib (CP-690, 550) is currently in clinical trials for RA with satisfactory effects and acceptable safety results. Our in vitro experiments have indicated that the inhibition effect could be mediated through the suppression of IL-17 and IFN-g production and proliferation of CD4+ T cells. Here, we document the in vitro, ex vivo and in vivo effects of a JAK inhibitor for the treatment of RA.
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