子痫前期是妊娠20 周以后出现的高血压和蛋白尿或器官功能障碍为主要表现的多系统综合征，是导致围产期母儿严重并发症和死亡率增高的重要原因之一。目前认为Thl7增加与子痫前期发病相关，我们前期的实验结果发现在子痫前期患者胎盘中EBI3保护性表达增加，而EBI3可以通过抑制Th17细胞分化在类风湿性关节炎减轻自身免疫反应，因此我们假设在子痫前期EBI3通过抑制Th17细胞分化重建母胎耐受。为了验证这一假说，我们建立了子痫前期小鼠模型，在子痫前期的不同阶段给予EBI3蛋白治疗，采用流式细胞术、酶联免疫吸附测定、免疫组化等手段，从分子、细胞、组织以及动物整体水平等多方面探讨EBI3在子痫前期中的作用，明确EBI3通过抑制Th17细胞分化对子痫前期小鼠模型免疫耐受的调节机制。本研究将从EBI3这个新视点为揭示子痫前期的免疫耐受重建机制奠定基础，为子痫前期的免疫防治提供新思路。

Preeclampsia is characterized by the presence of elevated blood pressures and proteinuria after 20 weeks of gestation or organ dysfunction as the main manifestation of the multiple system syndrome. It is a major cause of maternal and fetal morbidity and mortality worldwide. So far, the pathogenesis of preeclampsia is not clearly clarified, a growing body of evidence shows that the occurrence of preeclampsia is associated with Th17 predominance.Our previous experimental results found EBI3 protective expression in placenta of patients with preeclampsia, and EBI3 can inhibit Th17 cell differentiation in rheumatoid arthritis and reduce their autoimmune response, so we assume that in preeclampsia EBI3 by inhibiting Th17 cell differentiation reconstruction of maternal-fetal tolerance. To test this hypothesis, the preeclampsia mice model was established and EBI3 protein was given to the preeclampsia mice model in the different stages of preeclampsia. Using flow cytometry, enzyme-linked immunosorbent assay and immunohistochemical method, from the overall level of the molecules, cells, tissues, animals and other aspects we explore the role of EBI3 in preeclampsia and clarify the regulation mechanism of EBI3 inducing immune tolerance by inhibiting Th17 cell differentiation in preeclampsia mouse model. This study will reveal the mechanism of EBI3 immune tolerance reconstruction in preeclampsia from a new point of view and provide new ideas for the immune prevention and treatment of preeclampsia.