原发性肾病综合征（PNS）是引起我国儿童慢性肾功能衰竭的重要原发疾病，给患儿及家庭、社会带来极大的身心及经济负担。既往的T细胞功能紊乱即Th1/Th2失衡理论不能诠释PNS的发病机理。本课题组前期研究发现PNS患儿外周血单个核细胞中Th17细胞比例增高、Treg细胞比例降低、并且首次发现患儿血清及肾组织中IL-17因子mRNA表达和蛋白表达较正常对照显著增加，推测Th17/Treg细胞比例失衡、Th17/IL-17轴效应异常放大是导致肾小球足细胞损伤、产生大量蛋白尿的重要机制。因此本项目拟采用鼠肾脏足细胞株进行体外实验、阿霉素肾病大鼠进行体内实验，从Th17/IL-17-足细胞损伤-蛋白尿途径，以新的视角阐明儿童PNS的部分发病机制；以RNAi 基因沉默技术阻断IL-17基因表达，干预PNS的足细胞病变为防止早期肾小球硬化、改善预后寻找新的治疗途径。

The primary nephrotic syndrome (PNS) is one of the most important cause of children with chronic renal failure, and bring great physical and psychological burden to patients and their families. T cell dysfunction of Th1 / Th2 imbalance theory can not interpret the pathogenesis of PNS. Our previous studies found that Th17 cells increased in children with PNS, Treg cells reduced in children with PNS , and for the first time found a significant increase in cytokine IL-17 mRNA expression and protein expression in serum and renal tissue compared with normal control, Th17/Treg cell ratio imbalanced and Th17/IL-17 axis amplification effect is an important mechanism leading to podocyte injury , resulting in a large number of proteinuria . Therefore, this project intends to adopt podocyte cell in vitro experiments , rats with adriamycin nephrosis in vivo experiments to clarify the pathogenesis of PNS from a new perspective of Th17/IL-17- podocyte injury - proteinuria way ; RNAi technology was used to block the IL-17 gene expression , to prevent PNS podocytes intervention and prevent early glomerular sclerosis lesions .