Cellular crosstalk mediating immune evasion in pancreatic cancer microenvironment

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the fourth most common cause of death from cancer worldwide, with a poor 5-year survival rate of 6%. Immunity in PDAC patients is diminished and the associated immune evasion is an underinvestigated field. The microenvironment of pancreatic cancer is an intricate mesh-like network in which various resident cell populations are closely interacting. To understand the roles played by these cell types, we attempt to delineate the diversified components in pancreatic cancer microenvironment and their contributions in hampering immune escape. In sum, there are two tiers of force influencing the clinical outcome of patients with pancreatic cancer. The anti-tumor force includes CD8+ T cells, NK cells, M1-type macrophages, Th1 cells, and dendritic cells (DCs). The other force facilitates tumor cells to become free of attacks from immune system, including cancer cells, PSCs, M2-type tumor-associate macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), Tregs, and Th2 cells. Combined therapy to break the balance between the two forces maybe a promising strategy to benefit patients with pancreatic cancer.