Phenotypic and transcriptional profiling of regulatory T (T_reg) cells at homeostasis reveals that T cell receptor activation promotes T_reg cells with an effector phenotype (eT_reg) characterized by the production of interleukin-10 and expression of the inhibitory receptor PD-1. At homeostasis, blockade of the PD-1 pathway results in enhanced eT_reg cell activity, whereas during infection with Toxoplasma gondii, early interferon-γ upregulates myeloid cell expression of PD-L1 associated with reduced T_reg cell populations. In infected mice, blockade of PD-L1, complete deletion of PD-1 or lineage-specific deletion of PD-1 in T_reg cells prevents loss of eT_reg cells. These interventions resulted in a reduced ratio of pathogen-specific effector T cells: eT_reg cells and increased levels of interleukin-10 that mitigated the development of immunopathology, but which could compromise parasite control. Thus, eT_reg cell expression of PD-1 acts as a sensor to rapidly tune the pool of eT_reg cells at homeostasis and during inflammatory processes.

稳态调节性 T (T _reg ) 细胞的表型和转录分析表明，T 细胞受体激活可促进具有效应表型 (eT _reg ) 的 T _reg细胞，其特征是产生白细胞介素 10 和表达抑制性受体 PD-1。在稳态时，阻断 PD-1 通路会导致 eT _reg细胞活性增强，而在弓形虫感染期间，早期干扰素-γ 会上调与 T _reg细胞群减少相关的骨髓细胞 PD-L1 表达。在受感染的小鼠中，阻断 PD-L1、完全删除 PD-1 或​​ T _reg细胞中谱系特异性删除 PD-1 可防止 eT _reg细胞损失。这些干预措施导致病原体特异性效应 T 细胞：eT _reg细胞的比例降低，白细胞介素 10 水平增加，从而减轻了免疫病理学的发展，但可能会损害寄生虫控制。因此，PD-1 的 eT _reg细胞表达充当传感器，在稳态和炎症过程中快速调节 eT _reg细胞库。