CD38 symmetric dimethyl site R58 promotes malignant tumor cell immune escape by regulating the cAMP-GSK3β-PD-L1 axis.

ABSTRACT: In recent years, immunotherapy has emerged as an effective approach for treating tumors, with programmed cell death ligand 1 (PD-L1)/programmed cell death protein-1 (PD-1) immune checkpoint blockade (ICB) being a promising strategy. However, suboptimal therapeutic efficacy limits its clinical benefit. Understanding the regulation mechanism of PD-L1 expression is crucial for improving anti-PD-L1/PD-1 therapy and developing more effective tumor immunotherapy. Previous studies have revealed that resistance to PD-L1/PD-1 blockade therapy arises from the upregulation of CD38 on tumor cells induced by ATRA and IFN-β, which mediates the inhibition of CD8⁺ T cell function through adenosine receptor signaling, thereby promoting immune evasion.Yet, the precise role of CD38 in regulating P

SUBMITTER: Liang L 

PROVIDER: S-EPMC11462232 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature