PD-L1 on dendritic cells attenuates T cell activation and regulates response to immune checkpoint blockade

Qi Peng, Xiangyan Qiu, Zihan Zhang, Silin Zhang, Yuanyuan Zhang, Yong Liang, Jingya Guo, Hua Peng, Mingyi Chen, Yang-Xin Fu and Haidong Tang ()
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Qi Peng: Tsinghua University
Xiangyan Qiu: University of Texas Southwestern Medical Center
Zihan Zhang: Tsinghua University
Silin Zhang: Tsinghua University
Yuanyuan Zhang: Tsinghua University
Yong Liang: University of Texas Southwestern Medical Center
Jingya Guo: Chinese Academy of Science Key Laboratory for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Hua Peng: Chinese Academy of Science Key Laboratory for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
Mingyi Chen: University of Texas Southwestern Medical Center
Yang-Xin Fu: University of Texas Southwestern Medical Center
Haidong Tang: Tsinghua University

Nature Communications, 2020, vol. 11, issue 1, 1-8

Abstract: Abstract Immune checkpoint blockade therapies have shown clinical promise in a variety of cancers, but how tumor-infiltrating T cells are activated remains unclear. In this study, we explore the functions of PD-L1 on dendritic cells (DCs), which highly express PD-L1. We observe that PD-L1 on DC plays a critical role in limiting T cell responses. Type 1 conventional DCs are essential for PD-L1 blockade and they upregulate PD-L1 upon antigen uptake. Upregulation of PD-L1 on DC is mediated by type II interferon. While DCs are the major antigen presenting cells for cross-presenting tumor antigens to T cells, subsequent PD-L1 upregulation protects them from killing by cytotoxic T lymphocytes, yet dampens the antitumor responses. Blocking PD-L1 in established tumors promotes re-activation of tumor-infiltrating T cells for tumor control. Our study identifies a critical and dynamic role of PD-L1 on DC, which needs to be harnessed for better invigoration of antitumor immune responses.

Date: 2020
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DOI: 10.1038/s41467-020-18570-x

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