Dataset Information


CD80-CD28 signaling controls the progression of inflammatory colorectal carcinogenesis.

ABSTRACT: In patients with ulcerative colitis (UC) the cumulative risk of colon cancer is lower than the actual rate of dysplasia suggesting an efficient immune surveillance mechanism. Since the co-stimulatory molecule CD80 is overexpressed in dysplastic colonic mucosa of UC patients and T-cell activation entails effective costimulation, we aimed to evaluate the functional implication of CD80 signaling in colonic UC-associated carcinogenesis. In humans, we observed that the percentage of CD80+ and HLA-A+ IEC was increased in the dysplastic colonic mucosa of UC patients. In vitro, IEC activated CD8+ T-cells through a CD80-dependent pathway. Finally, in the AOM/DSS-induced colonic adenocarcinoma model CD80 signaling inhibition significantly increased the frequency and extension of high-grade dysplasia, whereas enhancing CD80 activity with an anti-CTLA4 antibody significantly decreased colonic dysplasia. In conclusion, CD80 signaling between IEC and T-cells represents a key factor controlling the progression from low to high grade dysplasia in inflammatory colonic carcinogenesis.

PROVIDER: S-EPMC4652987 | BioStudies |

REPOSITORIES: biostudies

Similar Datasets

| S-EPMC4891122 | BioStudies
| S-EPMC2809935 | BioStudies
| S-EPMC4932699 | BioStudies
| S-EPMC6509793 | BioStudies
| S-EPMC6791427 | BioStudies
| S-EPMC6708661 | BioStudies
| S-EPMC6176894 | BioStudies
| E-GEOD-37283 | BioStudies
| S-EPMC8327077 | BioStudies
2012-04-19 | E-GEOD-37283 | ArrayExpress