Reuschel Emma L, Wang JiangFang, Shivers Debra K, Muthumani Karuppiah, Weiner David B, Ma Zhengyu, Finkel Terri H
Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.
Division of Rheumatology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America.
PLoS One. 2015 Aug 24;10(8):e0136323. doi: 10.1371/journal.pone.0136323. eCollection 2015.
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.
REDD1是一种高度保守的应激反应蛋白，在多种细胞应激后会上调，包括缺氧、DNA损伤、能量应激、内质网应激和营养剥夺。最近，REDD1被证明参与地塞米松诱导的小鼠胸腺细胞自噬。然而，我们对REDD1在成熟T细胞中的功能知之甚少。在这里，我们首次表明，用PHA或CD3/CD28磁珠刺激T细胞后，REDD1会上调。尽管激活标志物看起来正常，但REDD1基因敲除的T细胞在增殖和细胞存活方面存在缺陷。这些发现证明了REDD1在T细胞功能中以前未被认识到的作用。
