Activation of T cell death-associated gene 8 attenuates inflammation by negatively regulating the function of inflammatory cells

被引：42
|
作者：
Onozawa, Yoshiko [1 ]
Komai, Tomoaki [1 ]
Oda, Tomiichiro [1 ]
机构：
[1] Daiichi Sankyo Co Ltd, Biol Res Labs 3, Edogawa Ku, Tokyo 1348630, Japan
来源：
EUROPEAN JOURNAL OF PHARMACOLOGY | 2011年 / 654卷 / 03期
关键词：
T cell death-associated gene 8; G-protein-coupled receptor; Knockout mouse; Anti-type II collagen antibody-induced arthritis; Delayed-type hypersensitivity; Collagen-induced arthritis; COLLAGEN-INDUCED ARTHRITIS; DELAYED-TYPE HYPERSENSITIVITY; EXTRACELLULAR ACIDIFICATION; MICE; ANTIBODY; IDENTIFICATION; TDAG8; INHIBITION; PSYCHOSINE; IL-1-BETA;
D O I：
10.1016/j.ejphar.2011.01.005
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
T cell death-associated gene 8 (TDAG8) is a G-protein-coupled receptor identified by differential mRNA display during thymocyte apoptosis induced by T cell receptor engagement. To examine the physiological role of an orphan G-protein-coupled receptor TDAG8 in inflammation, we studied various immune-mediated inflammatory disease models using TDAG8-deficient mice. We found that TDAG8-deficient mice showed significant exacerbation of anti-type II collagen antibody-induced arthritis and delayed-type hypersensitivity, and showed a slight exacerbation of collagen-induced arthritis. These results suggest that TDAG8 acts as a negative regulator of inflammation. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码：315 / 319
页数：5
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