HBV相关性HCC发病机制复杂，目前认为HBV所致的免疫炎性反应在HCC的发病中起重要作用。近年来发现的免疫细胞Th17及其分泌的IL-22涉及多种炎症性疾病及肿瘤。研究显示慢乙肝、HCC患者体内Th17细胞和IL-22均显著升高，促使炎症加剧和肿瘤发生。我们前期工作发现，IL-22可促肝细胞异常增殖，而且IL-22可抑制 HepG2细胞中的XRCC3，XRCC3遗传变异体rs861539单核苷酸多态性与HCC发病风险密切相关。然而在HBV感染环境中，哪种HBV抗原对Th17细胞作用最显著，这些分泌IL-22的Th17细胞有怎样的表型特征及功能，它们通过什么机制调节XRCC3基因促使HCC发生尚未明确。本项目拟通过体内外实验探讨HBV感染环境中IL-22+ Th17细胞调节XRCC3基因的机制，为慢乙肝，肝硬化，HCC逐步演变机制提供理论支持，为临床治疗提供干预靶标。

Pathogenesis of hepatocellular carcinoma(HCC) with HBV infection is extremely complicated. At present, immune inflammatory reaction induced by HBV has an important effect on the tumorigenesis of HCC. Recently, researchers have found Th17 cell and its secreting factor IL-22 involved in the pathogenesis of multiple inflammatory diseases and tumors. Some studies showed us that Th17 cell and IL-22 were significant up-regulation in the patients with hepatitis B and HCC. they aggravated the progress of inflammation and tumor. In our preliminary works, we found IL-22 could remarkably promote the proliferation of hepatic cell; And IL-22 inhibited the expression of XRCC3; rs861539 SNP of XRCC3 was statistically associated with HCC risk. However, it remains obscure which type of HBV antigens mainly affects Th17 cell, what the phenotypic characteristics and function of IL-22+ Th17 cell are, and how they modulate XRCC3 to prompt HCC progression. In this study, we want to investigate the mechanism of Th17 cell regulating XRCC3 via producing IL-22 in vivo and in vitro. These results will provide HBV-associated liver diseases progression from chronic liver inflammation, cirrhosis to HCC with theoretical support, and offer a new intervening target to clinic treatment.