Dataset Information


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 or PGE2 receptors EP2 and EP4 antagonists, combined with anti-PD-1 blockade was therapeutic in terms of improving eradication of tumors and augmenting the numbers of functional tumor-specific CTLs. Thus, COX2/PGE2 axis inhibition is a promising adjunct therapy to PD-1 blockade for immune-based therapies in cancer.

PROVIDER: S-EPMC5685710 | BioStudies |

REPOSITORIES: biostudies

Similar Datasets

| S-EPMC4505619 | BioStudies
| S-EPMC5623733 | BioStudies
2013-01-01 | S-EPMC3752535 | BioStudies
2021-09-13 | GSE160785 | GEO
| S-EPMC4552524 | BioStudies
| S-EPMC2731790 | BioStudies
| S-EPMC7772804 | BioStudies
| S-EPMC7282934 | BioStudies
| S-EPMC4877699 | BioStudies
| S-EPMC7611767 | BioStudies