干预肾间质炎症是防止肾间质损伤进展到终末期肾病（ESRD）的关键。众多患者对糖皮质激素和免疫抑制剂不敏感导致治疗失败，间充质干细胞具有免疫抑制和抗炎症作用，有望成为理想的免疫抑制新方法。CD4+ T细胞是介导肾间质炎症损伤的重要细胞。我们前期研究提示:骨髓间充质干细胞可通过改变CD4+T细胞的免疫反应性修复肾间质炎症，但是骨髓间充质干细胞由于其来源的有创性和数量少，限制其进一步临床应用。本研究拟以胎盘间充质干细胞（PMSC）替代骨髓间充质干细胞，移植给单侧输尿管结扎大鼠，观察其是否通过影响树突状细胞的功能和趋化因子的表达，进而影响CD4+T细胞向Th1、Th2、Th17、Treg 的分化格局及其相应细胞因子的表达，导致相应炎症细胞在肾脏的聚集改变，发挥修复肾间质炎症损伤的作用，阐明CD4+T细胞的极化在胎盘间充质干细胞修复肾间质炎症中的作用及机制，为PMSC治疗肾间质损伤寻找新的治疗靶点。

Intervention renal interstitial inflammation is crucial to the prevention from renal interstitial damage to end-stage renal disease (ESRD). For many patients, poor response to glucosteroids and immunosuppressive agents usually leads to failure in treatment. Mesenchymal stem cells are expected to be a novel way of immunosuppressive therapy for their immunosuppression and anti-inflammatory effects. CD4+ T cells play an important role in the mediation of renal interstitial inflammatory damage. Our previous research suggested bone marrow mesenchymal stem cells could repair renal interstitial inflammation by changing the immune reactivity of CD4+ T cells. Yet, the lack of origin and its invasive access limits its clinical application. This study is aimed to explore the role of CD4+ T cell polarization in repairing renal interstitial inflammation by placenta mesenchymal stem cells and its mechanism, and look for new therapeutic target for the management of renal interstitial injury with placenta mesenchymal stem cells (PMSC). We tried PMSC instead of bone marrow mesenchymal stem cells (BMSC) to investigate the effect of intravenously administered PMSC on renal interstitial inflammation. We hypothesis that PMSC may affect CD4+ cell differentiation to different subtypes by influencing the function of dendritic cells and chemokine expression, thus affecting the related inflammation factor expression and inflammatory cell infiltration in the kidney, and further help to repair kidney injury.