Id1 expression promotes peripheral CD4+ T cell proliferation and survival upon TCR activation without co-stimulation.
Id1 expression promotes peripheral CD4+ T cell proliferation and survival upon TCR activation without co-stimulation.
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DOI：
10.1016/j.bbrc.2013.05.054
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发表时间：
2013-06-21
影响因子：
3.1
通讯作者：
Zhang, Yu
中科院分区：
文献类型：
--
作者：
Liu, Chen;Jin, Rong;Wang, Hong-Cheng;Tang, Hui;Liu, Yuan-Feng;Qian, Xiao-Ping;Sun, Xiu-Yuan;Ge, Qing;Sun, Xiao-Hong;Zhang, Yu
虽然E蛋白在胸腺细胞发育中的作用已被充分证实，但对其在外周T细胞中的功能知之甚少。在这里，我们证明了由CD4启动子驱动的E蛋白显性负抑制因子Id1的转基因表达，可以替代CD28传递的共刺激信号，促进初始CD4+细胞在抗CD3刺激下的增殖和存活。我们进一步发现，在抗κ刺激后，表达ID1的细胞的IL-2产生和NF-CD3B活性显著增加，这可能至少部分地促进了其增殖和存活。综上所述，这项研究的结果表明E和ID蛋白在外周T细胞激活中起着重要作用。ID蛋白绕过共刺激信号使T细胞活化的能力在调节T细胞免疫方面具有重要意义。
Although the role of E proteins in the thymocyte development is well documented, much less is known about their function in peripheral T cells. Here we demonstrated that CD4 promoter-driven transgenic expression of Id1, a naturally occurring dominant-negative inhibitor of E proteins, can substitute for the co-stimulatory signal delivered by CD28 to facilitate the proliferation and survival of naïve CD4+ cells upon anti-CD3 stimulation. We next discovered that IL-2 production and NF-κB activity after anti-CD3 stimulation were significantly elevated in Id1-expressing cells, which may be, at least in part, responsible for the augmentation of their proliferation and survival. Taken together, results from this study suggest an important role of E and Id proteins in peripheral T cell activation. The ability of Id proteins to by-pass co-stimulatory signals to enable T cell activation has significant implications in regulating T cell immunity.
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