Blackburn Shawn D, Shin Haina, Freeman Gordon J, Wherry E John
Immunology Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15016-21. doi: 10.1073/pnas.0801497105. Epub 2008 Sep 22.
Programmed death-1 (PD-1) regulates T cell exhaustion during chronic infections. Blocking the PD-1:PD-ligand (PD-L) pathway reinvigorates exhausted CD8 T cells. Exactly how blocking PD-1:PD-L interactions improves T cell immunity, however, remains unclear. PD-1:PD-L blockade could reprogram all exhausted T cells to become antiviral effectors. Alternatively, this blockade might selectively expand a subset of exhausted T cells. We have identified two subpopulations of exhausted CD8 T cells during chronic viral infection in mice. One subset of exhausted CD8 T cells is rescued by alphaPD-L1 blockade, whereas the other subset appears more terminally differentiated and responds poorly to PD-1:PD-L blockade. Blocking PD-1:PD-L interactions reduces spontaneous apoptosis and enhances expansion and protective immunity of the rescuable subset, but not the more terminally differentiated subset of exhausted CD8 T cells. These results have implications for predicting clinical responses to PD-1-based therapeutic interventions and for understanding T cell dynamics during persisting infections.
程序性死亡蛋白 1(PD-1)在慢性感染期间调节 T 细胞耗竭。阻断 PD-1:PD 配体(PD-L)途径可使耗竭的 CD8 T 细胞恢复活力。然而,阻断 PD-1:PD-L 相互作用究竟如何改善 T 细胞免疫仍不清楚。PD-1:PD-L 阻断可能会使所有耗竭的 T 细胞重新编程成为抗病毒效应细胞。或者,这种阻断可能会选择性地扩增一部分耗竭的 T 细胞。我们在小鼠慢性病毒感染期间鉴定出了耗竭的 CD8 T 细胞的两个亚群。一部分耗竭的 CD8 T 细胞亚群可通过αPD-L1 阻断得到挽救,而另一亚群似乎分化程度更高,对 PD-1:PD-L 阻断反应不佳。阻断 PD-1:PD-L 相互作用可减少自发凋亡,并增强可挽救亚群的扩增和保护性免疫,但对耗竭的 CD8 T 细胞中分化程度更高的亚群则无此作用。这些结果对于预测基于 PD-1 的治疗干预的临床反应以及理解持续性感染期间的 T 细胞动态具有重要意义。