滋养细胞来源的CXCL16调节蜕膜巨噬细胞和γδ T细胞功能的分子机制

母-胎界面多种免疫细胞功能状态正常是维持免疫耐受微环境，保障正常妊娠，促进胎儿健康发育所不可或缺的重要因素。本课题组既往研究发现：滋养细胞来源的CXCL16能够募集单核细胞和γδT细胞到达蜕膜局部，蜕膜巨噬细胞呈现耐受表型。我们近期研究表明，滋养细胞来源的CXCL16能够诱导巨噬细胞（MΦ）向耐受型（M2型MΦ）转变，继而促使NK细胞的失活，且蜕膜γδ Τ细胞呈调节性Foxp3+表型。然而CXCL16是如何调节MΦ和γδ T细胞功能的，以及受到CXCL16调节的MΦ和γδ T细胞在维持正常妊娠中所发挥的作用及机制仍远未阐明。因此，本项目以体外模拟母-胎界面免疫微环境为研究手段，并借助体内动物模型，深入解析CXCL16调节MΦ和γδ T细胞功能的分子机理及其在维持正常妊娠中的作用。本项目将为进一步理解母-胎免疫调节机制，并以关键分子为靶点防治妊娠相关疾病提供有力的理论基础和科学依据。

The multiple immune cells function normally at the maternal-fetal interface is an indispensable factor for maintaining immune homeostasis, ensuring normal pregnancy, and promoting the healthy development of the fetus. Our group's previous studies found that trophoblast-derived CXCL16 can recruit monocytes and γδT cells to the decidua, and the decidual macrophages (MΦ) exhibit the tolerance phenotype. Our recent studies have found that CXCL16 can polarize MΦ to M2 type, which in turn promotes inactivation of NK cells, and the decidual γδ Τ cells exhibit a regulatory Foxp3+ phenotype. However, how CXCL16 regulates the function of MΦ and γδT cells and their role in maintaining normal pregnancy has not yet been elucidated. Therefore, this project uses in vitro simulation of the maternal-fetal interface immune microenvironment and in vivo animal models to analyze the molecular mechanisms of CXCL16 regulating MΦ and γδ T cell functions and its roles in maintaining normal pregnancy. This project will provide a powerful theoretical and experimental basis for further understanding the immune regulation at the maternal-fetal interface, and then targeting key molecules to prevent pregnancy-related diseases.