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.
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.