抗病毒天然免疫应答和炎症反应是机体应对病原微生物感染或组织损伤所启动的保护性反应。我们前期的研究结果表明菱形蛋白酶iRhom2与接头蛋白MITA相互作用，影响MITA稳定性，并促进DNA病毒感染诱导的I型干扰素表达。我们还发现iRhom2的缺失促进TNF和IL-1诱导的下游炎症因子表达。目前我们已经获得了iRhom2基因敲除小鼠。在本项目中，我们将利用该小鼠研究iRhom2在抗DNA病毒诱导的天然免疫与TNF或IL-1介导的炎症反应过程中的功能与分子机制。本项目的研究成果将为病毒感染或炎症反应引起的慢性或突发性疾病治疗提供新的分子靶标。

Antiviral immune response and inflammatory response are protective reactions initiated by pathogen infections or tissue injury. In our previous unpublished study, we found that rhomboid protease iRhom2 interacts with the adaptor protein MITA, influences its stability, and potentiates DNA virus-triggered type I interferon expression. Deletion of iRhom2 promotes TNF- and IL-1-induced expression of inflammatory factors. We have abtained the iRhom2 knockout mice. In this project, we will investigate molecular mechanisms responsible for DNA virus-triggered expression of type I IFNs and TNF/IL-1 triggered NF-kappa B activation mediated by iRhom2. This project will provide new candidate targets for the treatment of chronic or paroxysmal diseases caused by virus infection or inflammation.