封锁
免疫疗法
生物
CD8型
癌症研究
免疫检查点
细胞毒性T细胞
黑色素瘤
免疫系统
免疫学
受体
生物化学
体外
作者
Imran Siddiqui,Karin Schaeuble,Vijaykumar Chennupati,Silvia A. Fuertes Marraco,Sandra P. Calderon-Copete,Daniela Pais Ferreira,Santiago J. Carmona,Léonardo Scarpellino,David Gfeller,Sylvain Pradervand,Sanjiv A. Luther,Daniel E. Speiser,Werner Held
出处
期刊:Immunity
[Elsevier]
日期:2019-01-01
卷期号:50 (1): 195-211.e10
被引量:1003
标识
DOI:10.1016/j.immuni.2018.12.021
摘要
Checkpoint blockade mediates a proliferative response of tumor-infiltrating CD8+ T lymphocytes (TILs). The origin of this response has remained elusive because chronic activation promotes terminal differentiation or exhaustion of tumor-specific T cells. Here we identified a subset of tumor-reactive TILs bearing hallmarks of exhausted cells and central memory cells, including expression of the checkpoint protein PD-1 and the transcription factor Tcf1. Tcf1+PD-1+ TILs mediated the proliferative response to immunotherapy, generating both Tcf1+PD-1+ and differentiated Tcf1-PD-1+ cells. Ablation of Tcf1+PD-1+ TILs restricted responses to immunotherapy. Tcf1 was not required for the generation of Tcf1+PD-1+ TILs but was essential for the stem-like functions of these cells. Human TCF1+PD-1+ cells were detected among tumor-reactive CD8+ T cells in the blood of melanoma patients and among TILs of primary melanomas. Thus, immune checkpoint blockade relies not on reversal of T cell exhaustion programs, but on the proliferation of a stem-like TIL subset.
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