辅助性T细胞17(Th17)与调节性T细胞(Treg)的免疫失衡是动脉粥样硬化(AS)发病的重要原因之一。吲哚胺2,3-双加氧酶(IDO)是调节Th17/Treg免疫平衡的关键蛋白，其表达和活性受芳香烃受体(AhR)的调控。牙龈卟啉单胞菌(Pg)是牙周炎与AS关系中的关键，可能通过促进Th17/Treg失衡加剧AS，但具体机制还不清楚。我们前期研究发现AS患者IDO下调可能与Pg感染相关，Pg可影响T细胞分化，可能通过毒力因子牙龈素(Rgp)降低树突状细胞中AhR和IDO的表达。本项目中我们将研究：AS患者的AhR/IDO信号激活是否与T细胞平衡及Pg Rgp相关；体内研究Pg是否通过Rgp调控Th17/Treg平衡，从而影响AS发病；体外研究Rgp是否通过AhR/IDO信号轴改变T细胞分化，这一调节作用在AS中意义如何。本研究有望揭示牙周炎促AS的发病机制，为相关AS潜在干预提供靶点。

The immune imbalance between T helper 17 (Th17) cell and regulatory T cell (Treg) is one of the most important cause of atherosclerosis (AS). Indoleamine 2,3-dioxgenase (IDO) is the key protein in regulating the balance between Th17 and Treg. The expression and activity of IDO is regulated by arylhydrocarbon receptor (AhR). Porphyromonas gingivalis (Pg) plays a key role in the relationship between periodontitis and atherosclerosis (AS), which might promote the development of AS by regulating Th17/Treg imbalance. However, the mechanism is still unclear. In our previous study, we found that downregulation of expression of IDO might be related with Pg infection. Pg altered T cell differentiation. Moreover, Pg reduced AhR and IDO expression in dendritic cell through its virulence factor gingipain (Rgp). In this project, we aim to investigate the following questions: The association between AhR/IDO, Th17/Treg balance and Pg infection in atherosclerosis patients; the effect of Rgp in Pg regulating Th17/Treg balance during periodontitis associated AS; the potential role of Rgp in T cell differentiation and proliferation via AhR/IDO signaling axis. This project may shed light on the role and mechanism of between periodontitis and AS, and may provide novel molecular target for the prediction of periodontitis associated AS.