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Fig. 1 | Molecular Cancer

Fig. 1

From: The reciprocal regulation between host tissue and immune cells in pancreatic ductal adenocarcinoma: new insights and therapeutic implications

Fig. 1

Immune infiltration contributes to PDAC outcomes. PDAC tumor tissue has complex interactions with multiple immune cells, mainly T cells, MDSCs, macrophages and neutrophils. CD8+ T cells eliminate cancer cells by releasing IFNγ and TNFα. CD4+ T cells can be divided into Th1, Th2, and Th17 cells and Tregs. Th1 cells assist CD8+ T cells in antitumor immunity. Th2 cells, which can be reversed into Th1 cells, can drive cancer cell growth and fibroblast activation and can promote the transition of the M1 macrophage into the M2 phenotype. The function of Th17 cells is still not clear, but the functions of these cells mainly depend on IL-17. Tregs inhibit the cytotoxic function of CD8+ T cells via IL-6 and TGFβ. Both MDSCs and M2 macrophages suppress CD8+ T cell functions through the secretion of cytokines. M1 macrophages have antitumor functions that are mediated by releasing IL-12, IL-23, TNFα and NO. M2 macrophages promote tumor progression by secreting cytokines to affect tumor cells, fibroblasts and the vasculature. The role of neutrophils is not clear, but it is known that these cells can exert effects through IL-6 and MMP

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