肝癌免疫抑制的诱导机制研究较多，但是糖代谢重编程相关的诱导机制研究较少。我们前期研究工作在肝癌组织局部首次发现了具有免疫抑制功能的FOXP3+natural T细胞，并且TGF-β1能够体外诱导natural T细胞表达FOXP3。CD147作为一种肝癌相关抗原，通过糖代谢重编程等多种机制参与肝癌的发生和发展。在本研究中，我们拟通过TIL流式染色和癌组织免疫组织化学染色，对于肝癌组织局部淋巴细胞免疫抑制状态与肝癌细胞糖代谢重编程之间的相关性进行研究；通过不同CD147表达水平肝癌细胞株的构建及其与natural T细胞的共同培养实验、TGF-β1联合酸性刺激诱导natural T细胞表达FOXP3的体外细胞实验，对于CD147相关的糖代谢重编程引发的肝癌免疫抑制及相关机制进行研究。本研究旨在揭示诱导肝癌免疫抑制的糖代谢重编程相关诱导机制，为肝癌免疫治疗联合糖代谢干预治疗提供理论基础。

Mechanisms underlying immunosuppression induced in hepatocellular carcinoma (HCC) is widely investigated, but the role of reprogramming of glucose metabolism in it is not clear. We previously identified a FOXP3+CD3+CD56+ population with immunosuppressive function in cancer tissues of HCC, and transforming growth factor β1 (TGF-β1) could effectively induce FOXP3 expression in natural T (CD3+CD56+) cells in vitro. As a HCC associated antigen, CD147 plays an important role in tumorigenesis and progression through multiple mechanisms, including reprogramming of glucose metabolism. In this study, we aim to explore the correlation between immunosuppression induced in cancer tissues of HCC and the reprogramming of glucose metabolism via flow cytometric study to tumor infiltrating lymphocytes (TIL) and immunohistochemical assays to tissue specimens. Immunosuppression and associated mechanism induced by CD147-mediated glucose metabolic reprogramming in hepatocellular carcinoma is under investigation through establishment of different HCC cell lines with various level of CD147 expression and co-culture with natural T cells, and detection of induced expression of FOXP3 by addition of TGF-β1 combined with acidic stimulation in vitro. This study is designed to reveal an innovative mechanism involving reprogramming of glucose metabolism responsible for immunosuppression induced in HCC, thus providing a theoretical basis for tumor immunotherapy combined with glucose metabolism-targeting intervention treatment.