Targeting ERO1A enhances antitumor immune response by recruiting CD8+T cells and synergizing with PD-L1 blockade in liver cancer

This led to an increased infiltration of CD8+T cells into the immune microenvironment, enhancing the antitumor immune response. Furthermore, targeting ERO1A in liver cancer also upregulated type I interferon synthesis, activated the JAK-STAT pathway, and promoted programmed cell death ligand 1 (PD-L1) and MHC-Ⅰ expression. Using liver cancer animal models, we demonstrated that combination treatment with ERO1A inhibitor and PD-L1 inhibitor increased CD8+T cell infiltration and enhanced their function within the tumor microenvironment, resulting in synergistic antitumor effects.

Therefore, ERO1A represents a promising therapeutic target in liver cancer, potentially suitable for combination with immune checkpoint inhibitors to improve patient outcomes.