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

VIP拮抗剂VIP杂交物能增强巨噬细胞RAW264.7与结肠癌CT26细胞条件培养液孵育的M1相关基因和吞噬能力。在免疫缺陷的SCID小鼠中，VIP杂交物单独或与抗PD-1抗体联合使用与对照组相比可抑制CT26肿瘤的生长。对肿瘤浸润性白细胞的分析发现，VIP杂交体增加了CT26细胞的M1/M2比率和巨噬细胞吞噬功能。此外，Vipr2基因沉默或VPAC2激活影响结肠癌CT26细胞条件培养液孵育的RAW264.7细胞的极化。我们的结论是，VIP杂交物增强了巨噬细胞的功能，从而减少了肿瘤的生长。

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.