Targeted deletion of PD-1 in myeloid cells induces antitumor immunity.

ABSTRACT: PD-1, a T cell checkpoint receptor and target of cancer immunotherapy, is also expressed on myeloid cells. The role of myeloid-specific versus T cell-specific PD-1 ablation on antitumor immunity has remained unclear because most studies have used either PD-1-blocking antibodies or complete PD-1 KO mice. We generated a conditional allele, which allowed myeloid-specific (PD-1^f/fLysMcre) or T cell-specific (PD-1^f/fCD4cre) targeting of Pdcd1 gene. Compared with T cell-specific PD-1 ablation, myeloid cell-specific PD-1 ablation more effectively decreased tumor growth. We found that granulocyte/macrophage progenitors (GMPs), which accumulate during cancer-driven emergency myelopoiesis and give rise to myeloid-derived suppressor cells (MDSCs), express PD-1. In tumor-b

SUBMITTER: Strauss L 

PROVIDER: S-EPMC7183328 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature