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Significance Programmed cell death protein ligand 1 (PD-L1)–expressing cells mediate tumor evasion from immune system by suppressing activated T lymphocytes. A bioactive lipid prostaglandin E2 (PGE2 ) formed from arachidonic acid by COXs and PGE2 synthases (PGESs) facilitates both cancer inflammation and immune suppression. Here, we show that tumor cells can induce PD-L1 expression in bone marrow–derived cells by affecting PGE2 metabolism in hematopoietic cells. The tumor-induced PD-L1 expression was limited to the myeloid cell lineage and, specifically, to the macrophages and myeloid-derived suppressor cells. Collectively, the obtained results demonstrate that selective inhibition of PGE2 -forming enzymes COX2, murine PGES1, or genetic overexpression of PGE2 -degrading enzyme 15-hydroxyprostaglandin dehydrogenase could provide a novel approach to regulate both PGE2 levels and PD-L1 expression in cancer, thus alleviating the immune suppression and stimulating antitumor immune response.

COX2/mPGES1/PGE 2 pathway regulates PD-L1 expression in tumor-associated macrophages and myeloid-derived suppressor cells

COX2/mPGES1/PGE ₂ pathway regulates PD-L1 expression in tumor-associated macrophages and myeloid-derived suppressor cells