The synergistic effects of combined PD-1 and VIP blockade against CT26 colon cancer in mice

VIP拮抗剂VIP hybrid可增强巨噬细胞RAW264.7与结肠癌CT 26细胞条件培养液共同孵育后M1相关基因表达，并增强巨噬细胞的吞噬能力。在免疫缺陷的SCID小鼠中，与对照相比，VIP杂合体单独或与抗PD-1抗体组合减弱了CT 26肿瘤生长。对肿瘤浸润性白细胞的分析发现VIP杂合物增加了CT 26细胞的M1/M2比率和巨噬细胞吞噬作用。此外，Vipr 2基因沉默或VPAC 2激活影响与来自结肠癌CT 26细胞的条件培养基孵育的RAW 264. 7细胞的极化。我们得出结论，VIP杂交增强巨噬细胞功能，从而减少肿瘤生长。

VIP hybrid, a VIP antagonist, enhanced M1-related genes and increased phagocytic ability in macrophage RAW264.7 cells incubated with conditioned medium from colon cancer CT26 cells. In immunodeficient SCID mice, VIP hybrid alone or in combination with anti-PD-1 antibody attenuated CT26 tumor growth compared with the control. Analysis of tumor-infiltrating leukocytes found that VIP hybrid increased M1/M2 ratios and macrophage phagocytosis of CT26 cells. Moreover, Vipr2 gene silencing or VPAC2 activation affected the polarization of RAW264.7 cells incubated with conditioned medium from colon cancer CT26 cells. We concluded that VIP hybrid enhanced macrophage functions, thereby reducing tumor growth.