Figure 2.

Combining epigenetic drugs with immune checkpoint inhibitors. Persistent antigen stimulation and inflammatory factors in chronic inflammation can cause dysfunction of tumor-infiltrating T cells, up-regulation of immune checkpoints, and production of immune evasion, which are associated with epigenetic modifications. Anti-PD-1 relieves the inhibitory effect of the epidemic checkpoint on tumor cells and antigen presenting cells by blocking the binding of PD-1 to its ligands PD-L1 and PD-L2 in the tumor microenvironment. Epigenetic modifiers can enhance antigen presentation by tumor cells, thereby enhancing the immune effects of T cells. Moreover, epigenetic modifiers inhibitors, such as BET, can also inhibit the expression of PD-L1 on the surface of tumor cells and tumor-infiltrating immune cells. Moreover, EZH2 inhibitors prevent the conversion of CD4 T cells into Treg cells to up-regulate the immune response of other cells. Therefore, the combination therapy of epigenetic modifiers with immune checkpoint inhibitors embodies great advantages.