众所周知，慢性乙型肝炎是免疫失衡介导的疾病。目前研究发现，髓样树突状细胞（mDCs）功能缺陷是乙型肝炎患者免疫失衡的主要因素。我们前期工作发现，肝脏内mDC表达IL-23，IL-23的表达水平与HBsAg含量成正比，HBsAg能够诱导单核来源的DC分泌IL-23，DC通过甘露糖受体（MR）摄取HBsAg。然而，HBV抗原是通过什么机制诱导mDC产生IL-23，这些产生IL-23的mDC具有怎样的表型特征，通过什么机制调节HBV特异性CTL细胞免疫应答，这些问题都尚未明确。本研究拟通过体内外技术探讨HBV抗原刺激下mDCs产生IL-23的机制和对病毒特异性CTL细胞功能的调节作用。并通过细胞因子抗体阻断和特异性分子干扰技术，确定mDCs通过IL-23调节HBV特异性CTL的机制。本研究不但深化乙型肝炎免疫失衡的理论认识，而且为将来设计更为有效的乙肝治疗性药物提供理论指导。

As we all know, chronic hepatitis B disease is mediated by immune imbalance.Recently, it is the key factor that the function of mDCs defect in patients with hepatiits B. In our pre-studies, we found that the expression level of IL-23 in mDCs was higher in liver tissue with hepatitis B, the IL-23 level is significantly related with HBsAg of serum, IL-23 product from monocyte devived of DCs was induced by HBsAg and DCs intaked the HBsAg by MR.However, it is not addressed how HBV antigen induce the IL-23 product from mDCs, what is the phenotype of this IL-23 producing mDCs, and how these mDCs regulate the function of HBV specific CTLs. These issues are not yet clear.In this study, we want to expore the mechanism of IL-23 product from mDCs and the function of mDCs to HBV specitic CTLs by IL-23, and further confirm the mechanism of mDCs regulating HBV specific CTLs by antobody blockage and RNAi.Our results will expound that the regulation mechanism of mDCs to HSC by IL-23 in hepatitis B, and will promised to effectively prevent, delay, even interrupt the inflammatory response in liver with chronic hepatiits B.