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We characterized the murine NK cell subsets of the tumor microenvironment(TME)with low expressions of CD16 and NKG2D and investigated the chemokines that deter CD16~low NKG2D~low subsets.Our results demonstrated the activation of primary and KY-1 NK cell by ligands and found that exogenous CXCL10/interferon-gamma-induced protein 10(IP-10)and fractalkine(FKN)can up-regulate the expression of CD16 and NKG2D.Moreover,both IP-10 and FKN are shown to facilitate migration,adhesion and cytotoxicity of NK cell subsets of the TME,due to the up-regulated CD16 and NKG2D.Overall,our data provide a new path by which to enhance murine NK cell cytotoxic potential and improve the quality of NK cells of the TME.
We characterized the murine NK cell subsets of the tumor microenvironment (TME) with low expressions of CD16 and NKG2D and investigated the chemokines that deter CD16 ~ low NKG2D ~ low subsets. Our results demonstrated the activation of primary and KY-1 NK cell by ligands and found that exogenous CXCL10 / interferon-gamma-induced protein 10 (IP-10) and fractalkine (FKN) can up-regulate the expression of CD16 and NKG2D.Moreover, both IP-10 and FKN are shown to facilitate migration, adhesion and cytotoxicity of NK cell subsets of the TME, due to the up-regulated CD16 and NKG2D. Overall, our data provide a new path by which to enhance murine NK cell cytotoxic potential and improve the quality of NK cells of the TME.