REDD1 Is Essential for Optimal T Cell Proliferation and Survival

被引:28
|
作者
Reuschel, Emma L. [1 ,2 ]
Wang, JiangFang [1 ,2 ]
Shivers, Debra K. [1 ]
Muthumani, Karuppiah [3 ]
Weiner, David B. [3 ]
Ma, Zhengyu [1 ,2 ]
Finkel, Terri H. [1 ,2 ]
机构
[1] Childrens Hosp Philadelphia, Div Rheumatol, Philadelphia, PA 19104 USA
[2] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA
[3] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA
来源
PLOS ONE | 2015年 / 10卷 / 08期
关键词
MAMMALIAN TARGET; MTORC1; REPRESSOR; FEEDBACK-CONTROL; DNA-DAMAGE; STRESS; EXPRESSION; AUTOPHAGY; RAPAMYCIN; HYPOXIA; GENE;
D O I
10.1371/journal.pone.0136323
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
REDD1 is a highly conserved stress response protein that is upregulated following many types of cellular stress, including hypoxia, DNA damage, energy stress, ER stress, and nutrient deprivation. Recently, REDD1 was shown to be involved in dexamethasone induced autophagy in murine thymocytes. However, we know little of REDD1's function in mature T cells. Here we show for the first time that REDD1 is upregulated following T cell stimulation with PHA or CD3/CD28 beads. REDD1 knockout T cells exhibit a defect in proliferation and cell survival, although markers of activation appear normal. These findings demonstrate a previously unappreciated role for REDD1 in T cell function.
引用
收藏
页数:13
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