Eating self for not be eaten: Pancreatic cancer suppresses self-immunogenicity by autophagy-mediated MHC-I degradation

摘要

Autophagy inhibition potentiates anti-pancreatic cancer immunotherapy. Tumoral MHC-I contributes to TCR-mediated antigen recognition by T cells, while PD-1–PD-L1 interaction causes T cell dysfunction and immune evasion. MHC-I is degraded by autophagy in pancreatic cancer, and thus results in deficiency of antigen presentation and consequent ineffectiveness of immunotherapy. Combination of autophagy inhibitor and PD-1/PD-L1 blockade can improve therapeutic efficacy of pancreatic cancer, showing the potential to be a promising strategy for cancer therapy