论文部分内容阅读
子痫前期(preeclampsia,PE)是导致围产期母儿死亡的重要疾病,患者多表现出肾功能减退、胎儿生长受限、全身炎症反应状态和自身抗体的产生。既往的研究假说认为:滋养细胞侵袭受限导致胎盘缺血、缺氧,并引起母胎界面的免疫失衡,促炎性的CD4~+T细胞增多,而调节性T细胞(T regulatory cells,Tregs)减少,进而引发以氧化应激、促炎性细胞因子(如内皮素)、活性氧和自身抗体(如血管紧张素Ⅱ的1型受体的竞争性抗体)生成为主要特征的慢性炎症,这些因素共同作用,导致孕期血压升高。关于调节性免疫细胞对于PE病理过程作用的最新研究提示,通过输入Tregs细胞或输注白细胞介素-10的方法增加Tregs数量可以降低胎盘缺氧的妊娠大鼠模型的血压,为PE发病机制中炎症反应的病理过程奠定了充分的理论基础。
Preeclampsia (PE) is an important disease leading to perinatal maternal death. More patients show renal dysfunction, fetal growth restriction, systemic inflammatory response and autoantibodies. Previous research hypothesis that: trophoblast invasion led to the placenta ischemia, hypoxia, and cause maternal-fetal interface immune imbalance, proinflammatory CD4 ~ + T cells increased, and regulatory T cells (Tregs) Decrease, which in turn triggers chronic inflammation predominantly characterized by the generation of oxidative stress, pro-inflammatory cytokines such as endothelin, reactive oxygen species, and autoantibodies such as competitive antibodies to angiotensin II type 1 receptors, these Factors together, leading to elevated blood pressure during pregnancy. Recent studies on the role of regulatory immune cells in the pathophysiology of PE suggest that increasing the number of Tregs by introducing Tregs cells or transfused interleukin-10 may reduce the blood pressure in the rat model of hypoxic placental pregnancy, which is responsible for the pathogenesis of PE The pathological process of inflammatory response laid a solid theoretical foundation.