IL-17 induces the production of IL-16 in rheumatoid arthritis

被引:44
作者
Cho, Mi-La [1 ]
Jung, Young Ok [2 ]
Kim, Kyoung-Woon [1 ]
Park, Mi-Kyung [1 ]
Oh, Hye-Joa [1 ]
Ju, Ji-Hyeon [1 ]
Cho, Young-Gyu [1 ]
Min, Jun-Ki [1 ]
Kim, Sung-II [3 ]
Park, Sung-Hwan [1 ]
Kim, Ho-Youn [1 ]
机构
[1] Catholic Univ, Coll Med, Rheumatism Res Ctr, Dept Internal Med,Div Rheumatol, Seoul 137701, South Korea
[2] Hallym Univ, Kang Nam Sacred Heart Hosp, Dept Internal Med, Div Rheumatol, Seoul 150950, South Korea
[3] Pusan Natl Univ, Coll Med, Dept Internal Med, Pusan 602739, South Korea
关键词
interleukin-16; interleukin-17; rheumatoid arthritis; synovial membrane; Toll-like receptors;
D O I
10.3858/emm.2008.40.2.237
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 fibroblast-like 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 beta, IFN-gamma, 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 beta, and IFN-gamma. 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 dose-dependently, whereas LIPS, 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.
引用
收藏
页码:237 / 245
页数:9
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