蜕膜巨噬细胞（dMφ）是母胎界面免疫耐受网络的核心成员，在孕早期呈免疫耐受表型M2型，其表型功能异常如何诱发妊娠失败迄今仍不明晰。近来我们发现母胎界面存在一群具有独特功能表型的巨噬细胞FLT-1+ dMφ，且蜕膜基质细胞（DSC）可分泌PLGF训导dMφ向M2型分化，提示PLGF/FLT-1在调节dMφ倾向耐受表型中发挥重要作用，但其分子机制尚不清楚。基于此本课题以FLT-1+dMφ独特功能表型的维持机制为切入口，通过体外模拟母胎界面局部微环境，并借助FLT-1(TK)-/-鼠等体内实验，研究1）母-胎界面PLGF表达调控机制；2）PLGF/FLT-1信号诱导dMφ向耐受表型分化的分子机制;3）母胎界面FLT-1+dMφ异常缺乏导致自然流产的病理机制，以期更深层次地剖析母胎免疫耐受机制，探讨蜕膜局部DSC对dMφ的“训导”机制;为自然流产等母胎免疫调节紊乱相关性疾病的临床防治提供理论依据。

Human decidual macrophage (dMφ) is an essential constituent of fetomaternal immunoregulation. M2 macrophages are the predominant phenotype in the decidua. However, the regulatory mechanism of its differentiation and polarization remains unclear. Our recent study shows that decidual PLGF/FLT-1 interaction promotes the polarization of M2 macrophage (such as high expression level of CD209 and TGFβ1, low expression level of CD86 and IL-1β) and suggests that PLGF may play a pivotal role in maternal-fetal tolerance. Therefore, our study aims to investigate 1) The regulation mechanism of PLGF expression at maternal fetal interface during early pregnancy; 2) The mechanism of PLGF/FLT-1 regulation in dMφ polarization and differentiation; 3) The pathological mechanism between abnormal low PLGF/FLT-1 expression and pregnancy loss. We hope this study can help in understanding the dialogue between decidual stromal cells and dMφ, the mechanism of maternal-fetal immune tolerance, as well as the prevention of spontaneous abortion.