免疫功能紊乱是重症休克发生发展的关键环节；肠淋巴液回流是休克后多器官损伤的重要因素；休克肠淋巴液与免疫功能紊乱的关系有待深入研究。肿瘤坏死因子α诱导蛋白8样分子2是维持机体免疫动态平衡的关键性蛋白，与休克发生过程中的免疫功能紊乱以及失控的全身炎症反应密切相关。本研究拟在前期工作基础上，应用小鼠失血性休克模型，从细胞和整体水平，体内、外实验探讨休克肠淋巴液对CD4+T细胞介导的细胞免疫功能的影响及与TIPE2的内在联系；应用慢病毒包装的TIPE2特异干扰RNA，沉默TIPE2基因表达，以TLR2/TLR4为切入点，深入探讨TIPE2在休克淋巴液调节T细胞免疫功能中的分子机制，阐明TIPE2在休克肠淋巴液调节T细胞免疫功能中的重要作用。最终揭示以TIPE2为干预靶点，能够减轻休克肠淋巴液导致的免疫功能紊乱，为失血性休克的免疫调控途径提供新思路。

A lot of animal experiments and clinical trials have proven that dysregulation of immune response has been involved in the pathogenetic mechanism of shock. Previous studies have demonstrated that post-shock mesenteric lymph (PSML) is an important mechanism of dysfunction of the cellular immunity followed by the development of hemorrhagic shock. Tumor necrosis factor-α (TNF-α) induced protein 8 like-2(TIPE2) plays an important regulatory role in the maintenance of immune homeostasis. Mice with hemorrhagic shock were used as a model system. In the present study, we will investigate the effects of drainage of post-shock mesenteric lymph on the expression of TIPE2, Toll-like receptor 4 (TLR4), TLR2 and other molecules in the signal pathway associated with TLR2/TLR4. The aim of study is to determine whether TIPE2 decreases the immune dysfunction induced by post-shock lymph via the silencing of TIPE2 gene expression, which will therefore indicate its critical role against hemorrhagic shock. Moreover, we will demonstrate the molecular mechanisms of immune dysfunction of shock induced by PSML through the TIPE2 from the cellular and molecular levels. Finally, we will provide a better understanding with regard to the mechanism of regulatory function of TIPE2 on the immune response in pathophysiological procedure of shock.