I 型干扰素在抗HBV固有免疫中具有重要作用，因此研究pDC中IFN-α的产生机制，有利于宿主清除HBV。在前期研究，我们在未治疗的慢性乙型肝炎患者外周血单个核细胞中发现：线粒体DNA(mtDNA)拷贝数与HBV血清标志物浓度密切相关；cGAS和STING蛋白表达量增高。那么HBV感染时，pDC中mtDNA能否激活cGAS-STING-TBK1-IRF3信号通路，促进I型干扰素表达？为明确这科学问题，本课题拟通过磁珠分选HBV患者pDC和构建mtDNA损伤的pDC细胞模型，对cGAS和STING基因进行过表达和干扰调控，观察pDC中mtDNA形态及数量和IFN-α的表达水平的变化情况，在此基础上进一步讨论mtDNA介导cGAS-STING-TBK1-IRF3信号通路在抗HBV固有免疫中的价值。本课题研究有利于认识pDC中I 型干扰素的产生机制，进一步为治疗HBV研究提供新的思路和靶点。

Type I interferon (IFN) plays an important role in innate immunity of anti Hepatitis B virus (HBV). Therefore, study to explore the mechanism of IFN-α production in pDCs is favorable for the host to clear HBV. In the previous study, we have found that mitochondrial DNA (mtDNA) copies were associated with concentration of HBV marker in peripheral blood mononuclear cells of untreated chronic hepatitis B patients, and the expression of cGAS and STING was increased. However, whether mtDNA could activate cGAS-STING-TBK1-IRF3 signaling pathway in pDCs, and promote the expression of type I interferon is still unknown. In order to clarify this problem, this project intends to collect HBV patient pDCs isolated by magnetic beads sorting and build the mtDNA damaged pDCs model, further to overexpress and interfere the expression of pDCs and STING genes, and to observe the changes of mtDNA morphology and quantity and IFN-α expression in pDCs. On the basis of this, we finally discuss the value of mtDNA-mediated cGAS-STING-TBK1-IRF3 signaling pathway in anti-HBV innate immunity. The finding of the study is expected to deepen the mechanism of type I interferon in pDCs, which provide new ideas and targets for the treatment of HBV.