ArticleMolecular therapy. Oncology2026
Rapidly evolved PD-1 for enhance receptor and checkpoint inhibitor in immunotherapy.
Article in Molecular therapy. Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
PD-1 is a crucial molecule indispensable for maintaining immune homeostasis. Disrupting the interaction between PD-1 and its ligands can significantly enhance the immune system's ability to combat tumors. By integrating the PD-1 ligand-binding domain with the CD28 signal fragments (switch molecule) on T cells, we can utilize co-stimulatory signals to boost the function of T cells while removing the inhibition of immune checkpoint molecules. However, the extensive application of anti-PD-1 monoclonal antibodies in clinical settings may neutralize the PD-1 switch molecule, thereby restricting its therapeutic potential. In this study, we used sequential mutation and sorting techniques to rapidly evolve a PD-1 molecule that exhibits high affinity for PD-L1 while avoiding the recognition by five of the six clinically approved anti-PD-1 drugs. Experimental results verify that the Fc fusion protein and switch receptor based on such PD-1 mutant enhance the efficacy of therapeutic T cells.
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