肝脏缺血再灌注损伤（Ischemia-reperfusion injury, I/RI）是一个复杂的病理生理过程，血流的阻断及氧运输的减少导致炎症反应并最终引起器官损伤。导致肝脏I/R损伤的因素很多，确切的发病机制尚不十分清楚 。本组预实验中发现阻断Toll样受体4(Toll like receptor 4，TLR4)能够减轻肝脏I/RI，另外通过回输体外诱导的Treg能够抑制炎性细胞因子IL-17等来减轻肝脏I/RI。TLR4与Treg，Th17在缺血再灌注中是否有联系仍不清楚。本项目通过干预TLR4信号来分析在体外TLR4信号对诱导Treg和Th17产生的影响；再通过肝脏缺血再灌注模型分析TLR4在体内对Treg/Th17平衡的影响。本项目的成功有利于发现缺血再灌注损伤中先天免疫和继发免疫之间的可能联系，为临床采取干预措施提供理论依据。

Ischemia-reperfusion injury, I/RI,is a complex pathological physiology process, the blocking blood flow and oxygen transportation decreases has lead to flammatory reaction and eventually cause organ damage.There are many factors Lead to liver I/R damage, but the exact pathogenesis is still unclear.This group of the experiment find that block the Toll like receptor 4 (TLR4) can reduce the liver I/RI,In addition, reinfusion in vitro-induced Treg can inhibit inflammatory cells factor IL-17 to reduce the liver I/RI.TLR4 and Treg,Th17 in ischemia-reperfusion whether any contact is still nuclear.This project through interpose TLR4 signal to analysis the TLR4 signal in vitro to the induction Treg and Th17 influence;And then analysis the influence of TLR4 in vivo to Treg/Th17 balance in the hepatic ischemia-reperfusion model.The success of this project to found a possible link between the innate immune and Secondary immune in the Ischemia-reperfusion injury,for clinical interventions to provide the theory basis.