Survival and maintenance of regulatory T cells require the kinase TAK1

作     者：Jae-Hoon Chang Hongbo Hu Shao-Cong Sun 

作者机构：Department of Immunology The University of Texas MD Anderson Cancer Center 7455 Fannin Street Box 902 Houston TX 77030 USA Center for Inflammation and Cancer The University of Texas MD Anderson Cancer Center 7455 Fannin Street Box 902 Houston TX 77030 USA The University of Texas Graduate School of Biomedical Sciences at Houston Houston TX 77030 USA College of Pharmacy Yeungnam University Gyeongsan 712- 749 Republic of Korea 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2015年第12卷第5期

页      面：572-579页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 07[理学] 1001[医学-基础医学(可授医学、理学学位)] 071009[理学-细胞生物学] 

基　　金：the National Research Foundation of Korea Grant funded by the Korean Government Jae-Hoon Chang and National Institutes of Health to Shao-Cong Sun supported by the 2013 Yeungnam University Research Grant the NIH/NCI-supported resources (flow cytometry, DNA analysis, histology, and animal facilities)under award 

主　　题：regulatory T cells autoimmunity TAK1 IKK Foxp3 

摘      要：Regulatory T （Treg） cells play a central role in regulating peripheral immune tolerance and preventing autoimmunity. Despite the extensive studies on the development of Treg cells, the molecular mechanisms that maintain the population of committed Treg cells remain poorly understood. We show here that Treg-conditional ablation of the kinase TAK1 reduced the number of Treg cells in the peripheral lymphoid organs, causing abnormal activation of conventional T cells and autoimmune symptoms. Using an inducible gene knockout approach, we further demonstrate that TAK1 is crucial for the survival of Treg cells. Expression of a constitutively active IKB kinase partially restored the level of Treg cells in the TAKITreg-KO mice. These results suggest a crucial role for TAK1 for maintaining the survival of committed Treg cells under physiololzical conditions.