Immune surveillance of nascent cancer cells is a fundamental process mediated by T-cells, macrophages, and natural killer cells that work to protect host against the unrestrained proliferation of transformed cells. Full T-cell activation requires the engagement of T-cell receptors with specific major histocompatibility complexes at the surface of antigen-presenting cells in the presence of adequate co-stimulatory signals provided by CD80 or CD86. Oncogenic insults inducing CD80 expression seem then to be able to modulate the anti-tumor immune response. The significant overexpression of CD80 in the colonic mucosa of patients with ulcerative colitis (UC) and dysplasia as opposed to CD80 down-regulation in non-inflammatory colon cancer have led to the hypothesis that the lack of positive co-stimulatory molecules is one of the main mechanisms by which colorectal cancer (CRC) escapes immune surveillance. The molecular mechanisms underlying immune surveillance remain, nevertheless, largely unknown.
Drug targets for cancer: CD80 research reagents
Other vital drug targets for cancer likeCD80:
Scarpa M, Scarpa M, Castagliuolo I, et al. CD80 down-regulation is associated to aberrant DNA methylation in non-inflammatory colon carcinogenesis. BMC Cancer. 2016;16:388.