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 CD 16~~w NKG2Dl^w subsets. Our results demonstrated t...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 CD 16~~w NKG2Dl^w 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 CD 16 and NKG2D. Moreover, both IP-10 and FKN are shown to facilitate migration, adhesion and cyto- toxicity of NK cell subsets of the TME, due to the up-regu- lated 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.展开更多
基金the National Natural Science Foundation of China (81171975)the Tianjin Institutes for Basic Sciences (15JCYBJC26900)
文摘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 CD 16~~w NKG2Dl^w 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 CD 16 and NKG2D. Moreover, both IP-10 and FKN are shown to facilitate migration, adhesion and cyto- toxicity of NK cell subsets of the TME, due to the up-regu- lated 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.