Abstract
Comment on: Lévy et al., Nat Cell Biol. 2015 Aug; 17(8):1062-73.
Highlights
Colorectal cancer (CRC) results from a series of histological changes, known as the ‘adenoma-carcinoma’ sequence, each accompanied by alterations to a specific oncogene or tumor suppressor gene
We investigated the mechanism underlying the induction of Cd8+ T-cell infiltration by the inhibition of intestinal epithelial cells (IECs) autophagy further
We found that autophagy inhibition changed the composition of the gut bacterial community, increasing the permeability of the intestinal barrier, with bacteria present in the crypt compartment
Summary
Colorectal cancer (CRC) results from a series of histological changes, known as the ‘adenoma-carcinoma’ sequence, each accompanied by alterations to a specific oncogene or tumor suppressor gene. Anti-CD8 antibody treatment abolished the protective antitumoral response mediated by autophagy deficiency in Apc+/-Atg7-/- mice, whereas CD4 depletion had no such effect. We investigated the mechanism underlying the induction of Cd8+ T-cell infiltration by the inhibition of IEC autophagy further. The inhibition of IEC autophagy has been shown to downregulated host immunity by decreasing the antimicrobial defenses mediated by Paneth and goblet cells 6.
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