Disruption of Rig-I in Mice Triggers Colitis Partially through Down-regulation of Gai2

作     者：Yi Wang~1 Hong-Xin Zhang~1 Zi-Xing Liu~1 Yue-Ping Sun~1 Xue-Song Liu~1 Long Wang~2 Shun-Yuan Lu~2 Hui Kong~3 Qiao-Ling Liu~3 Xi-Hua Li~1 Zhen-Yu Lu~1 Sai-Juan Chen~2 Zhu Chen~2 Shi-San Bao~4 Wei Dai~5 Zhu-Gang Wang~(1-4*) 1.Department of Medical Genetics,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China 2.State Key Laboratory of Medical Genomics,Rui-Jin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China 3.Shanghai Research Center for Model Organisms,Shanghai 201203,China 4.Department of Pathology,University of Sydney,Sydney,2570 NSW,Australia 5.Department of Environmental Medicine,New York University School of Medicine,Tuxedo,NY 10987,USA 

会议名称：《中国遗传学会“发育、遗传和疾病”研讨会》

会议日期：2007年

学科分类：1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学] 

关 键 词：Knockout Mice Gene Regulation Inflammation 

摘      要：RIG-I（Retinoid acid-inducible gene-I）,a putative RNA helicase with cytoplasmic caspase-recruiting domain（CARD）,is identified as a pattern recognition receptor（PRR）mediating antiviral immunity by inducing type I interferon *** further study the biological function of RIG-I,we generated Rig-Imice through homologous recombination by taking different strategy from previously ***-Imice are viable and *** analysis shows that Rig-Imice develop a colitis-like phenotype spontaneously and also increased susceptibility to DSS-induced colitis. Accordingly,the size and number of Peyer s patches dramatically decreased in mutant *** peripheral T cell subsets in mutant mice were characterized by an increase in effector T cells and decreased na（?）ve T cells,indicating an important role of Rig-I in the regulation of T cell *** was further found that Rig-I deficiency leads to down-regulation of Gai2 expression in various tissues including T and B *** contraries,up-regulation of Rig-I in NB4 cells treated with ATRA is accompanied by elevated Gai2 ***,Gai2 promoter activity is increased in co-transfected NIH3T3 cells in a Rig-I dose-related *** these findings suggest that Rig-I plays the crucial roles in the regulation of Gai2 expression and T cell *** development of colitis may be,at least in part,associated with down-regulation of Gai2 and disturbed T cell homeostasis.