AI Article Synopsis
- The PD-L1/PD-1 immune checkpoint is a key target for cancer treatment, as PD-L1 can inhibit T cell activation and allow tumors to evade the immune system.
- Therapeutic methods that block the interaction between PD-L1 and PD-1 can enhance the immune response against tumors.
- Recent research emphasizes the importance of post-translational modifications (PTMs) of PD-L1, such as glycosylation and phosphorylation, in regulating its stability and function, which could provide new avenues for cancer therapies aimed at overcoming immune evasion.
Article Abstract
The immune checkpoint, programmed death 1 ligand-1/programmed death -1 (PD-L1/PD-1), is one of the most promising targets for tumor immunotherapy. Overexpressed PD-L1 on the surface of tumor cells could bind to PD-1 on the surface of T cells and inhibit the T cell activation, triggering tumor-immune-escape; therapeutic strategies targeting PD-1/PD-L1 restore the cytotoxic function of immune cells in the tumors by blocking PD-1/PD-L1 interaction. The PD-L1 undergoes multi-level regulations in tumor cells. Among them, post-translational modifications (PTMs) of PD-L1 mainly including glycosylation, phosphorylation, ubiquitination, acetylation and palmitoylation, have attracted much attention in recent years. These modifications directly affect the stability, cellular localization and function of PD-L1, and subsequently regulate the T cell activation and tumor immunity. Therefore, intervention with PTMs of PD-L1 may serve as a new approach for anti-tumor immunity-escape therapy.
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