Graphical abstract. (IMAGE)
Caption
IFN-γ-driven HLA-E upregulation mediates immune evasion in the hepatocellular carcinoma (HCC) tumor microenvironment. Tumor-infiltrating lymphocytes (TILs) release IFN-γ, which binds to the IFN-γ receptor on HCC cells and activates JAK signaling, leading to STAT3 phosphorylation. Phosphorylated STAT3 translocates to the nucleus and promotes the transcriptional upregulation of HLA-E, resulting in increased HLA-E expression on the tumor cell surface. Surface HLA-E engages the inhibitory receptor CD94/NKG2A on NK cells, thereby suppressing cytotoxicity and facilitating immune evasion.
Credit
Zhao Shu, Junfeng Guo, Lin Lv, Zhenxiang Peng, Shengtao Liao, Chuanfei Li, Zhechuan Mei
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CC BY-NC-ND