HBXIP靶向TBK1负向调控I型干扰素生成及其机制研究

病毒感染后固有免疫反应的核心是Ｉ型干扰素的产生和抗病毒状态的建立。细胞质核酸免疫识别信号通过不同的受体识别细胞质核酸后都需通过关键激酶TBK1介导下游干扰素的生成，因而通过调控TBK1的活性能够直接影响宿主细胞的抗病毒固有免疫。研究发现，自噬在抗病毒免疫应答过程中发挥作用。我们前期的研究结果发现HBXIP能够抑制I型干扰素的产生，并且HBXIP和TBK1能够相互作用，提示HBXIP能够促进TBK1的自噬性降解。本项目拟在前期结果的基础上，进一步研究HBXIP通过促进TBK1的选择性自噬降解抑制I型干扰素产生的机制。

The core of innate immune response after viral infection is the production of type I interferon and the establishment of antiviral state. After cytoplasmic nucleic acid immune recognition signals recognize cytoplasmic nucleic acid through different receptors, they all need to mediate the production of downstream interferon through key kinase TBK1. Therefore, the antiviral innate immunity of host cells can be directly affected by regulating the activity of TBK1. Studies have found that autophagy plays a role in the process of antiviral immune response. Our previous study found that HBXIP can inhibit the production of type I interferon, and HBXIP can interact with TBK1, suggesting that HBXIP can promote the autophagic degradation of TBK1. Based on the previous results, this project intends to further study the mechanism of HBXIP inhibiting the production of type I interferon by promoting the selective autophagic degradation of TBK1.