Abstract
Abstract The effectiveness of cancer immunotherapies targeting co-inhibitory molecules CTLA-4 and PD-1 have fully validated that reversal of tumor immune tolerance is an important new pathway for the treatment of tumor. Recent evidence shows that NK cell exhaustion in HBV related HCC patients. However, the underlying mechanism remains unclear. In our study, we found that the expression of NKG2A on NK cells from peripheral blood and different tissue regions of HCC was significantly increased, which then impaired NK cell-mediated cytotoxic capacity and interferon-γ production. We further found the same inhibition and exhaustion of NK cell in the different disease-progressing groups of HCC patients. Furthermore, we confirmed that IL-10 amounts in the immune microenvironment of hepatitis and HCC were highly related to the development of HCC. This study will help to understand the mechanism of immune tolerance of NK cells induced by HCC and verify the potential value of NKG2A as a novel intervention target for cancer immunotherapy.
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