Tumor-necrosis factor-α induces retinoic acid-inducible gene-I in rheumatoid fibroblast-like synoviocytes

被引:21
|
作者
Imaizumi, Tadaatsu [1 ]
Matsumiya, Tomoh [1 ]
Yoshida, Hidemi [1 ]
Naraoka, Takuya [2 ]
Uesato, Ryoko [2 ]
Ishibashi, Yasuyuki [2 ]
Ota, Ken [3 ]
Toh, Satoshi [2 ]
Fukuda, Shinsaku [3 ]
Satoh, Kei [1 ]
机构
[1] Hirosaki Univ, Grad Sch Med, Dept Vasc Biol, Hirosaki, Aomori 0368562, Japan
[2] Hirosaki Univ, Grad Sch Med, Dept Orthopaed Surg, Hirosaki, Aomori 0368562, Japan
[3] Hirosaki Univ, Grad Sch Med, Dept Gastroenterol & Haematol, Hirosaki, Aomori 0368562, Japan
基金
日本学术振兴会;
关键词
Fibroblast-like synoviocytes; RA; TNF-alpha; IFN-beta; RIG-I; CCL5; DOUBLE-STRANDED-RNA; INTERFERON-GAMMA; RIG-I; ENDOTHELIAL-CELLS; EPITHELIAL-CELLS; TNF-ALPHA; EXPRESSION; ARTHRITIS; INVOLVEMENT; INDUCTION;
D O I
10.1016/j.imlet.2008.12.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tumor-necrosis factor-alpha (TNF-alpha) is a potent proinflammtory cytokine and a key molecule in the pathogenesis of rheumatoid arthritis (RA). Retinoic acid-inducible gene-I (RIG-I) is a DExH box protein, which is known to play a role in the inflammatory and immune reactions. We previously reported about potential involvement of RIG-I in synovial inflammation in RA. In the present study, we demonstrated the expression of RIG-I in fibroblast-like synoviocytes stimulated with TNF-alpha. RNA interference against interferon (IFN)-beta abolished theTNF-alpha-induced RIG-I expression. In addition, knockdown of RIG-I partially inhibited the TNF-alpha-induced expression of CC chemokine ligand (CCL) 5, a chemokine with chemotactic activity toward lymphocytes and monocytes. These findings suggest that the TNF-alpha/IFN-beta/RIG-I/CCL5 pathway may be involved in the pathogenesis of synovial inflammation in RA. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:89 / 93
页数:5
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