tumor suppression by pd-1/pd-l1 interaction blockage in mice model

Background: overexpression of programmed cell death ligand 1 (pd-l1) in tumor cells and subsequent interaction with the programmed cell death protein 1 (pd-1) in tumor-infiltrating t cells cause an immune evasion of the tumor from cytotoxic t-cells. therefore, inhibiting such interaction by a recombinant pd-1 can hinder tumor growth and extend the survival rate. methods: the mouse extracellular domain of pd-1 (mpd-1) was expressed in e. coli bl21 (de3) strain and purified using nickel affinity chromatography. the binding ability of the purified protein to human pd-l1 was studied using elisa. finally, the tumor-bearing mice were used to evaluate the potential antitumor effect. results: the recombinant mpd-1 showed a significant binding capacity to human pd-l1 at the molecular level. the tumor size significantly decreased in the tumor-bearing mice after the intra-tumoral injections of mpd-1. moreover, the survival rate increased significantly after eight weeks of monitoring. the histopathology revealed the necrosis in the tumor tissue of the control group compared to the mpd-1 received mice. conclusions: our outcomes propose that interaction blockade between pd-1 and pd-l1 is a promising approach for targeted tumor therapy.