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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Revealing the crosstalk between nasopharyngeal carcinoma and immune cells in the tumor microenvironment

Fig. 1

Mechanisms of immune escape in nasopharyngeal carcinoma. EBV-encoding miRNA mediates the escape of the NK cell killing by down-regulating the expression of ligands to NKG2D. NPC cells also secrete factors such as TGF-β to inhibits the recruitment of APCs, and meanwhile, secret several chemokines to recruit immunosuppressive regulatory T cells (Treg). Tregs further inhibit the function of APCs through the binding of CTLA-4 to CD86 and releases suppressive cytokines such as IL-10 to activated effector T cells (Teff), prohibiting their cytotoxicity to NPC. Its expression of membrane-bound TGF-β also inhibits the action of NKs. NPC cells directly inhibit the action of Teff by expressing PD-L1 ligand, which induce T cell anergy upon binding to PD-1. Secretion of exosomes containing LMP1, miRNA, Galectin1 and Galectin 9 leads to disfunction of Teff and NK

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