肝细胞肝癌（Hepatocellular carcinoma, HCC）是一类诊疗困难、死亡率高的恶性肿瘤。急需新靶点、新方法来提高临床治疗水平。CD317在HCC中表达上调，但对疾病发展尤其是肿瘤免疫逃逸的作用尚不清楚。研究发现，CD317通过ILT7受体抑制类浆树突状细胞（Plasmacytoid dendritic cells，pDCs）活化，CD317胞外段蛋白具有抗炎、抑制哮喘的功能。我们也发现，CD317胞外段蛋白能结合于NK细胞、T细胞表面，而靶细胞表面CD317具有抑制NK细胞体外杀伤功能的作用，提示CD317是一个外源性免疫抑制蛋白，可能促进肿瘤免疫逃逸。但截至目前尚没有这方面的报道。因此，本项目拟以肿瘤免疫为关注点，探讨肝癌细胞CD317通过抑制肝脏免疫应答促进HCC发生发展的作用及其分子机制，为HCC诊疗手段开发提供新的思路。

Hepatocellular carcinoma (HCC) is one of the most common cancers with high mortality due to limited diagnostic and therapeutic options. Identification of prognostic markers and development of novel therapeutic approaches are critically important. CD317 is upregulated in HCC with unclear function. As reported, CD317 is a novel ligand for an immune receptor called immunoglobulin-like transcript 7 (ILT7) and plays a key role in the regulation of plasmacytoid dendritic cells (pDCs) activation. Recombinant CD317-ECD (extracellular domain) can suppress airway inflammation in mouse models of mild chronic asthma and allergen-induced acute exacerbation of asthma. Otherwise, we also found that recombinant CD317-ECD can interact with unclear receptors expressed in NK cells and T cells. CD317 directly inhibits the cytolyticactivity of NK cells in vitro. Accordingly, we speculate that CD317 may serve as an exogenous immune inhibitory protein that may be involved in tumor immune escape. However, there is no literature reported regarding whether and how CD317 participated in tumor immune escape. Hence, in this study, we plan to elucidate the role and mechanism of tumor-derived CD317 in the regulation of liver immune response during HCC development, which may provide new information for HCC diagnosis and therapy.