T细胞受体
FOXP3型
细胞生物学
生物
转录因子
T细胞
调节性T细胞
信号转导
自身免疫
白细胞介素2受体
免疫学
CD8型
细胞毒性T细胞
ZAP70型
CD28
效应器
基因
免疫系统
遗传学
作者
Andrew J. Levine,Aaron Arvey,Wei Jin,Alexander Y. Rudensky
出处
期刊:Nature Immunology
[Springer Nature]
日期:2014-09-28
卷期号:15 (11): 1070-1078
被引量:397
摘要
Regulatory T cells help to keep adaptive immunity in check. Rudensky and colleagues show that these cells continuously require TCR signaling to maintain their cellular identity and homeostasis and to exert their suppressive ability. Foxp3+ regulatory T cells (Treg cells) maintain immunological tolerance, and their deficiency results in fatal multiorgan autoimmunity. Although heightened signaling via the T cell antigen receptor (TCR) is critical for the differentiation of Treg cells, the role of TCR signaling in Treg cell function remains largely unknown. Here we demonstrated that inducible ablation of the TCR resulted in Treg cell dysfunction that could not be attributed to impaired expression of the transcription factor Foxp3, decreased expression of Treg cell signature genes or altered ability to sense and consume interleukin 2 (IL-2). Instead, TCR signaling was required for maintaining the expression of a limited subset of genes comprising 25% of the activated Treg cell transcriptional signature. Our results reveal a critical role for the TCR in the suppressor capacity of Treg cells.
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