Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Nat Immunol. 2011 Jun;12(6):478-84. doi: 10.1038/ni.2018.
Weak T cell antigen receptor (TCR) signals from contact with self ligands act in synergy with antiapoptotic signals induced by interleukin 7 (IL-7) to promote the survival of naive T cells in a resting state. The amount of background TCR signaling in naive T cells is set by post-thymic TCR tuning and operates at an intensity just below that required to induce entry into the cell cycle. Costimulation from higher concentrations of IL-7 and other common γ-chain cytokines can induce T cells to undergo homeostatic proliferation and conversion into cells with a memory phenotype; many of these memory phenotype cells may be the progeny of cells responding to self antigens. The molecular mechanisms that control the conversion of naive resting T cells into memory-phenotype cells TCR-dependent in normal animals are beginning to be understood.
与自身配体接触的弱 T 细胞抗原受体 (TCR) 信号与白细胞介素 7 (IL-7) 诱导的抗凋亡信号协同作用,促进静止状态下初始 T 细胞的存活。初始 T 细胞中背景 TCR 信号的数量由胸腺后 TCR 调节设定,并以刚好低于诱导细胞进入细胞周期所需的强度运行。来自较高浓度的 IL-7 和其他共同 γ 链细胞因子的共刺激可以诱导 T 细胞进行稳态增殖并转化为具有记忆表型的细胞;其中许多记忆表型细胞可能是对自身抗原产生反应的细胞的后代。控制正常动物中初始静止 T 细胞向记忆表型细胞转化的分子机制 TCR 依赖性正在开始被理解。