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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: J Immunol. 2016 Aug 1;197(3):691–698. doi: 10.4049/jimmunol.1600458

Figure 1. Cancer and immune cell interactions during tumor progression.

Figure 1

(1) Differential recruitment of various immune cell types is modulated by the tumor microenvironment (TME). (2) Tumor associated macrophages (TAMs), neutrophils, and Monocytes are converted to an anti-inflammatory phenotype. (3) M2 TAMs in conjunction with Myeloid derived suppressor cells (MDSCs) help drive EMT in the TME. These recruited cells also help suppress tumor infiltrating lymphocytes. (4) Upon successful EMT, cells can maintain this phenotype via autocrine complement protein C3a production and (5) blocks complement mediated cytotoxicity by upregulating CD59. (6) MDSCs can help metastasis formation by secreting versican to help the reverse process of mesenchymal to epithelial transition (MET) and seed the premetastatic niche at the distant site from the primary tumor. Increased PDL-1 and tumor autophagy aids in blocking cytotoxic T cell (CTL) (7) synapse formation and cytotoxicity. (8) This metastatic process can be limited by NK cell mediated cytotoxicity by targeting upregulated NKG2D ligands.