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

来源：

IMMUNOLOGY LETTERS | 2009年 / 122卷 / 01期

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

页码：89 / 93

页数：5

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