KMID : 0620920080400020237
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Experimental & Molecular Medicine 2008 Volume.40 No. 2 p.237 ~ p.245
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IL-17 induces the production of IL-16 in rheumatoid arthritis
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Cho Mi-La
Park Mi-Kyung Kim Kyoung-Woon Ju Ji-Hyeon Min Jun-Ki Park Sung-Hwan Jung Young-Ok Kim Ho-Youn Oh Hye-Joa Cho Young-Gyu Kim Sung-Il
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Abstract
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The purpose of this study was to investigate the expression of IL-16 in the rheumatoid synovium and the role of inflammatory cytokines and Toll-like receptor (TLR) ligands in IL-16 production by fibroblastlike synoviocytes (FLS) of rheumatoid arthritis (RA) patients. Immunohistochemical staining was performed with a monoclonal antibody to IL-16 in synovial tissues from patients with RA and likewise in patients with osteoarthritis (OA). FLS were isolated from RA synovial tissues and stimulated with IL-15, IL-1¥â, IFN-¥ã, and IL-17. The IL-16 mRNA level was assessed by semiquantitative RT-PCR and real time (RT) PCR and a comparison was made between IL-16 mRNA levels produced by RA-FLS and OA-FLS. Production of IL-16 was identified by a western blot assay, and IL-16 production after stimulation by specific ligands of TLR2 and TLR4 was assessed by RT-PCR. While immunohistochemical staining demonstrated strong expression of IL-16 mRNA in synovial tissues from patients with RA, similar findings were not present in the OA group. Moreover, mRNA expression of IL-16 by RA-FLS increased after treatment with IL-17 but not with IL-15, IL-1¥â, and IFN-¥ã. Specifically, IL-17 increased IL-16 mRNA level by RA-FLS and peripheral blood mononuclear cells in a dose-dependent manner. However, IL-17 did not stimulate IL-16 production in OA-FLS. Peptidoglycan, a selective TLR2 ligand, also increased production of IL-16 by RA-FLS dosedependently, whereas LPS, a selective TLR4 ligand, had no such stimulatory effect. The results from our data demonstrate that IL-17 and TLR2 ligands stimulate the production of IL-16 by RA-FLS.
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KEYWORD
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interleukin-16, interleukin-17, rheumatoid arthritis, synovial membrane, Toll-like receptors
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