Division of Immunology and Allergy, Department of Medicine, Lausanne University Hospital (CHUV), 1011 Lausanne, Switzerland.
Ludwig Center for Cancer Research, Department of Fundamental Oncology, University of Lausanne, 1066 Epalinges, Switzerland.
Immunity. 2016 Aug 16;45(2):415-27. doi: 10.1016/j.immuni.2016.07.021.
Chronic infections promote the terminal differentiation (or "exhaustion") of T cells and are thought to preclude the formation of memory T cells. In contrast, we discovered a small subpopulation of virus-specific CD8(+) T cells that sustained the T cell response during chronic infections. These cells were defined by, and depended on, the expression of the transcription factor Tcf1. Transcriptome analysis revealed that this population shared key characteristics of central memory cells but lacked an effector signature. Unlike conventional memory cells, Tcf1-expressing T cells displayed hallmarks of an "exhausted" phenotype, including the expression of inhibitory receptors such as PD-1 and Lag-3. This population was crucial for the T cell expansion that occurred in response to inhibitory receptor blockade during chronic infection. These findings identify a memory-like T cell population that sustains T cell responses and is a prime target for therapeutic interventions to improve the immune response in chronic infections.
慢性感染会促进 T 细胞的终末分化(或“耗竭”),并被认为会阻止记忆 T 细胞的形成。相比之下,我们发现一小部分病毒特异性 CD8(+) T 细胞在慢性感染期间维持着 T 细胞反应。这些细胞由转录因子 Tcf1 的表达所定义,并依赖于 Tcf1 的表达。转录组分析表明,这群细胞具有中央记忆细胞的关键特征,但缺乏效应细胞特征。与传统的记忆细胞不同,表达 Tcf1 的 T 细胞表现出“耗竭”表型的特征,包括表达抑制性受体,如 PD-1 和 Lag-3。这群细胞对于慢性感染期间抑制性受体阻断后 T 细胞的扩增至关重要。这些发现确定了一种类似记忆的 T 细胞群体,它维持着 T 细胞反应,是改善慢性感染中免疫反应的治疗干预的主要目标。