Under lymphopenic conditions, the rapid spontaneous proliferation produces cells that robustly differentiate into effector memory T (T_EM) cells, and the aberrant expansion is preferentially driven by self-antigens. The pool size of effector memory T-cell is governed by a complex homeostatic balance between proliferation and death. Perp is a critical effector involved in the p53-dependent apoptotic pathway and widely expressed in mammalian tissues. We have previously shown that Perp has a prominent role in activation-induced cell death of peripheral Th17 cells. Here, we show that Peripheral Perp^−/−CD4⁺ T_EM cells outcompete wild type T_EM cells for access to splenic niches in vivo. The skewing of the Perp^−/− T_EM cells compartment was not the result of a difference in lymphopenia-induced proliferation, but the resistance to apoptosis, particularly after anti-Fas treatment. Data presented in this work indicate that Perp mediates the persistence of CD4⁺ T_EM cells in irradiation-induced lymphopenic settings.

在淋巴细胞减少的条件下，快速的自发增殖产生可牢固分化为效应记忆T（T _EM）细胞的细胞，异常扩增优先由自身抗原驱动。效应记忆T细胞的库大小受增殖和死亡之间复杂的稳态平衡控制。Perp是参与p53依赖性细胞凋亡途径的关键效应子，在哺乳动物组织中广泛表达。我们以前已经表明，Perp在激活诱导的外周Th17细胞死亡中具有重要作用。在这里，我们显示外围Perp ^-/- CD4 ⁺ T _EM细胞胜过野生型T _EM在体内进入脾壁的细胞。Perp ^-/- T _EM细胞区室的倾斜不是淋巴细胞减少引起的增殖差异的结果，而是对细胞凋亡的抵抗力的结果，尤其是在抗Fas治疗后。这项工作中提供的数据表明，Perp在辐射诱导的淋巴细胞减少环境中介导了CD4 ⁺ T _EM细胞的持久性。