CK2B Induces CD8⁺ T-Cell Exhaustion through HDAC8-Mediated Epigenetic Reprogramming to Limit the Efficacy of Anti-PD-1 Therapy in Non-Small-Cell Lung Cancer.

ABSTRACT: Anti-PD-1 therapy has left an indelible mark in the field of non-small-cell lung cancer (NSCLC) treatment; however, its efficacy is limited in clinical practice owing to differences in the degree of effector T-cell exhaustion. Casein kinase 2 (CK2) is a protein kinase that plays an important role in T-cell immunity. In this study, it is aimed to explore the potential of targeting CK2 and its regulatory subunit CK2B to prevent or reverse T-cell exhaustion, thereby enhancing the efficacy of anti-PD-1 therapy in NSCLC. In this study, it is found that CK2B expression is closely associated with T-cell exhaustion as well as the efficacy of anti-PD-1 therapy based on scRNA-seq and in vitro and in vivo experiments. Utilization of CK2 inhibitors or knockdown of CK2B expression can upregulate TBX21

SUBMITTER: Liu S 

PROVIDER: S-EPMC12021095 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature