宿主炎症小体的功能状态与病原微生物的致病性密切相关，一方面炎症小体复合物的适度激活具有杀灭病原体以及限制感染等作用；另一方面，过度的炎症反应会导致多种组织、器官的伤害，甚至危及生命，因此炎症小体复合物需要精确的调控，筛选和鉴定新的炎症小体复合物的调控分子对于抗病原微生物感染具有重要的意义。我们前期研究发现E3泛素连接酶Traf3能够与ASC发生相互作用，Traf3可以显著上调ASC介导的IL-1β的分泌。在LPS刺激下，Traf3敲除细胞中pro-Caspase1的切割及其IL-1β的水平明显低于野生型细胞，且ASC由细胞核到细胞质的穿梭明显减弱。我们拟进一步研究Traf3与ASC的相互作用及其相互作用的生理意义，揭示Traf3作为E3连接酶参与炎症小体信号通路的分子机制，在此基础上阐明RLRs、TLRs和NLRs这三个信号通路之间交联的分子机理，并有可能为抗细菌药物的开发提供潜在的靶点。

The cells of the innate immune system mobilize a coordinated immune response towards invading microbes. These immune responses typically lead to infection control and tissue repair. Exaggerated or uncontrolled immune responses, however, can also induce acute of chronic inflammatory pathologies that are characteristic for many common diseases such as sepsis, arthritis, atherosclerosis, or Alzheimer's disease. Therefore, research on the exact molecular mechanisms of activation inflammasome for most is of vital importance. Our previous work showed that Traf3 associates with ASC to regulate inflammasome signaling. Traf3-/- mouse macrophages were deficient in caspase-1 cleavage and IL-1β secretion, with lower ASC nuclear to cytoplasm translocation. Taken together, we would like to explore the interaction of Traf3 with ASC and their biological significance, elucidating the molecular mechanism of Traf3 in inflammasome activation, providing a novel potential for bacteria therapy.