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Tumor Suppression by PD-1/PD-L1 Interaction Blockage in Mice Model
Shima Salehi1, Hajarossadat Ghaderi1, Mahdi Habibi-Anbouhi2
1Biotechnology Research Center, Venom and Biotherapeutics Molecules Laboratory, Pasteur Institute of Iran, Tehran, Iran.
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.
Insights
Blocking the interaction between programmed cell death protein 1 (PD-1) and programmed cell death ligand 1 (PD-L1) with recombinant PD-1 effectively reduced tumor growth and improved survival rates in mice.
Area of Science:
- Immunology
- Oncology
- Biotechnology
Background:
- Tumor cells evade immune detection via PD-L1/PD-1 interactions, suppressing T-cell activity.
- Targeting this pathway offers a strategy to restore anti-tumor immunity.
Purpose of the Study:
- To investigate the therapeutic potential of a recombinant mouse PD-1 (mPD-1) protein.
- To assess its ability to block PD-L1 and inhibit tumor growth.
Main Methods:
- Recombinant mPD-1 was expressed in E. coli and purified.
- Binding affinity to human PD-L1 was confirmed via ELISA.
- Antitumor efficacy was evaluated in tumor-bearing mice.
Main Results:
- mPD-1 demonstrated significant binding to human PD-L1.
- Intra-tumoral mPD-1 injections led to decreased tumor size.
- Survival rates increased, and tumor necrosis was observed.
Conclusions:
- Blocking the PD-1/PD-L1 interaction is a viable strategy for targeted cancer therapy.
- Recombinant PD-1 shows promise as an anti-tumor agent.
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