The mechanisms by which trophoblast-derived molecules induce maternal–fetal immune tolerance

作     者：Xiao-Qiu Wang Da-Jin Li Xiao-Qiu Wang;Da-Jin Li

作者机构：Laboratory for Reproductive ImmunologyKey Laboratory of Reproduction Regulation of NPFPCSIPPRShanghai Key Laboratory of Female Reproductive Endocrine Related DiseasesHospital and Institute of Obstetrics and GynecologyIRDFudan University Shanghai Medical CollegeShanghaiChina 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志(英文版))

年 卷 期：2020年第17卷第11期

页      面：1204-1207页

核心收录：

学科分类：1002[医学-临床医学] 100211[医学-妇产科学] 10[医学] 

基　　金：supported by grant number MOST 2017YFC1001400 awarded to D.-J.L grants from the National Natural Science Foundation of China,numbers 81971456 and 81200425 awarded to X.-Q.W grants from the National Natural Science Foundation of China,numbers 81471548 and 81490744 awarded to D.-J.L 

主　　题：placental tissuesat maternal immune system maternal fetal tolerance suppression maternal immune rejection decidual stromal placentationdelicate crosstalk maternal fetal interfacethe trophoblast derived molecules 

摘      要：A successful pregnancy requires the maternal immune system to recognize and tolerate the allogeneic fetus while maintaining defense against infection both systemically and in placental *** the maternal–fetal interface,the trophoblasts in the placenta play an essential role in the suppression of maternal immune rejection of the *** ensure maternal–fetal tolerance and successful placentation,delicate crosstalk is established among fetus-derived trophoblasts,maternal immune cells,and decidual stromal cells(DSCs)during normal *** immune cells not only participate in the maintenance of immune tolerance but also regulate the function of trophoblasts to promote fetal *** imbalance in this crosstalk may lead to adverse pregnancy outcomes,such as recurrent spontaneous abortion,preeclampsia,preterm birth,intrauterine growth restriction,and *** we outline some of the important discoveries in recent years related to the mechanisms by which trophoblast-derived molecules induce maternal–fetal immune tolerance.