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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Tumor immune microenvironment-based therapies in pancreatic ductal adenocarcinoma: time to update the concept

Fig. 2

Interactions between PDAC cells and myeloid cells in TIME. A IL-17 receptor activation of tumor cells promotes the recruitment and activation of TANs through a variety of downstream secreted factors. TANs interact with tumor cells through TNF/TNFR, leading to the production of more chemokines. Activated TANs promote liver metastasis of PDAC by releasing Gas6 to bind to AXL on the surface of tumor cells. B Tumor cells promote TAM polarization toward the M2 phenotype by secreting tumor-promoting factors to activate receptors such as CSF1R and CCR2 on TAMs. The recognition of CD47/SIRPα enables tumor cells to acquire the ability of anti-phagocytosis. TAMs can also activate proliferative genes in tumor cells. C Tumor cells actively secrete GM-CSF and many other factors to recruit and activate MDSCs. Activated MDSCs secrete a variety of tumor-promoting factors to further induce tumor proliferation. D Tumor cells inhibit the activation and normal function of DCs. Red arrows represent tumor-promoting processes. Pink circles represent possible treatment strategies. TAN: tumor‐infiltrating neutrophil; TNF: tumor necrosis factor; Gas6: growth arrest specific 6; TAM: tumor-associated macrophage; GARP: Glycoprotein A repetitions predominant; MDSC: myeloid-derived suppressor cell; HIF: hypoxia-inducible factor; ROS: reactive oxygen species; Arg-1: arginase-1; iNOS: inducible nitric oxide synthase; IRF8: interferon regulatory factor-8

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