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.

中文翻译：

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正常 T 细胞稳态：幼稚细胞转化为记忆表型细胞。

来自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) 诱导的抗细胞凋亡信号协同作用，以促进静止状态下幼稚 T 细胞的存活。幼稚 T 细胞中的背景 TCR 信号量由胸腺后 TCR 调整设置，并以略低于诱导进入细胞周期所需的强度运行。来自更高浓度 IL-7 和其他常见 γ 链细胞因子的共刺激可诱导 T 细胞进行稳态增殖并转化为具有记忆表型的细胞；许多这些记忆表型细胞可能是对自身抗原作出反应的细胞的后代。开始了解正常动物中控制幼稚静息 T 细胞转化为 TCR 依赖性记忆表型细胞的分子机制。