Prostaglandin E₂ and PD-1 mediated inhibition of antitumor CTL responses in the human tumor microenvironment.

ABSTRACT: Accumulating evidence indicates that inflammation plays a critical role in cancer development; however, mechanisms of immunosuppression hinder productive anti-tumor immunity to limit immunopathology. Tumor-specific cytotoxic T lymphocyte (CTL) dysfunction or exhaustion by upregulating inhibitory receptors such as programmed cell death 1 (PD-1) in tumor-bearing hosts is one such mechanism. Identification and blockade of the pathways that induce CTL dysfunction has been shown to partially restore CTL function in tumor-bearing hosts. Cyclooxygenase-2 (COX-2) is a rate-limiting enzyme for prostanoid biosynthesis, including prostaglandin E₂ (PGE₂), and plays a key role in both inflammation and cancer. The disruption of COX2/PGE2 signaling using COX₂ inhibitors o

SUBMITTER: Miao J 

PROVIDER: S-EPMC5685710 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature