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CD8 +  T-cell exhaustion is a dysfunctional state that is regulated through the expression of inhibitory checkpoint receptor genes including the cytotoxic T-lymphocyte–associated antigen 4, programmed death 1, and DNA methylation of effector genes interferon-γ, perforin, and granzyme B. Different strategies have been used to reverse T-cell exhaustion, which is an adverse event of checkpoint inhibitor blockade. Here, we present the mechanisms by which DNA methyltransferase inhibitors and Simian virus 40 large T antigen through viral mimicry can promote the reversion of exhausted CD8 +  T cells. We examine how these pharmacological strategies can work together to improve the clinical efficacy of immunotherapies.

Checkpoint inhibitor blockade and epigenetic reprogrammability in CD8+ T-cell activation and exhaustion

Checkpoint inhibitor blockade and epigenetic reprogrammability in CD8⁺ T-cell activation and exhaustion