Expression of interleukin-10 family cytokines in rheumatoid arthritis

نویسنده

  • Tiina Alanärä
چکیده

Background and aims: Interleukin-10 (IL-10) is an anti-inflammatory cytokine, and its expression is increased in rheumatoid arthritis (RA). A number of novel cytokines have been found recently, which have been designated as the IL-10 family based on their genetic characteristics. These cytokines include IL-19, IL-20, IL-22, IL-24 and IL-26. Information concerning the expression and function of these cytokines is restricted. The aim of this study was to investigate the expression of these cytokines in rheumatoid arthritis, and to characterize more specifically the expression patterns of cytokines that are elevated in rheumatoid joints. Methods: mRNA expression of cytokines in leucocytes was studied by quantitative reverse transcriptase PCR (Q-RT-PCR). The levels of intracellular IL-19 protein were studied by flow cytometry. The effect of IL-19 protein on the expression of other cytokines was studied by ELISA. Peripheral blood, synovial fluid and synovial tissue samples from patients with RA, peripheral blood samples from healthy volunteers and synovial tissue samples from patients with osteoarthritis were studied. Results: Elevated levels of IL-10, IL-22 and IL-22R1 were observed in the peripheral circulation of patients with RA. In addition, IL-10, IL-19 and IL-22BP were found to be upregulated in SFMC of patients with RA. Increased expression of IL-19 was also observed in RA synovial tissues. Macrophages were found as primary source for IL-19 expression in RA synovium. The expression of intracellular IL-19 protein was also upregulated in samples of patients with RA. However, IL-19 did not markedly change the expression pattern of other cytokines in vitro. Conclusions: Most of the IL-10 family cytokines and their receptor subunits can be detected in RA. In addition to IL-10, IL-19 levels were increased in rheumatoid joints. Further functional studies are needed to determine the significance of the altered expression of IL-19 in the pathogenesis of RA.

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تاریخ انتشار 2007