CD8⁺ T cells responding to infection differentiate into a heterogeneous population composed of progeny that are short-lived and participate in the immediate, acute response and those that provide long-lasting host protection. Although it is appreciated that distinct functional and phenotypic CD8⁺ T cell subsets persist, it is unclear whether there is plasticity among subsets and what mechanisms maintain subset-specific differences. Here, we show that continued Id2 regulation of E-protein activity is required to maintain the KLRG1^hi CD8⁺ T cell population after lymphocytic choriomeningitis virus infection. Induced deletion of Id2 phenotypically and transcriptionally transformed the KLRG1^hi “terminal” effector/effector-memory CD8⁺ T cell population into a KLRG1^lo memory-like population, promoting a gene-expression program that resembled that of central memory T cells. Our results question the idea that KLRG1^hi CD8⁺ T cells are necessarily terminally programmed and suggest that sustained regulation is required to maintain distinct CD8⁺ T cell states.

对感染做出反应的CD8 ⁺ T 细胞分化成异质群体，由寿命短并参与即时、急性反应的后代和提供持久宿主保护的后代组成。尽管人们认识到不同的功能和表型 CD8 ⁺ T 细胞亚群持续存在，但尚不清楚亚群之间是否存在可塑性以及维持亚群特异性差异的机制。在这里，我们表明，在淋巴细胞性脉络膜脑膜炎病毒感染后，维持 KLRG1 ^hi CD8 ⁺ T 细胞群需要 Id2 对 E 蛋白活性的持续调节。诱导Id2缺失，在表型和转录上将 KLRG1 ^hi “末端”效应/效应记忆 CD8 ⁺ T 细胞群体转化为 KLRG1 ^lo记忆样群体，促进类似于中枢记忆 T 细胞的基因表达程序。^{我们的结果质疑 KLRG1 hi} CD8 ⁺ T 细胞必然被最终编程的观点，并表明需要持续调节来维持不同的 CD8 ⁺ T 细胞状态。