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.

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.

Blocking Tim-3 enhances the anti-tumor immunity of STING agonist ADU-S100 by unleashing CD4 T cells through regulating type 2 conventional dendritic cells.

An immunosuppressive tumor microenvironment (TME) is a major obstacle in tumor immunotherapy. Stimulator of interferon genes (STING) agonists trigger an inflammatory innate immune response to potentially overcome tumor immunosuppression. While STING agonists may hold promise as potential cancer therapy agents, tumor resistance to STING monotherapy has emerged in clinical trials, and the mechanisms remain unclear.