Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
Front Immunol. 2019 Mar 26;10:573. doi: 10.3389/fimmu.2019.00573. eCollection 2019.
Semi-allogenic fetuses are not rejected by the maternal immune system because feto-maternal tolerance induced by CD4CD25FoxP3 regulatory T (Treg) cells is established during pregnancy. Paternal antigen-specific Treg cells accumulate during pregnancy, and seminal plasma priming plays an important role in expanding paternal antigen-specific Treg cells in mouse models. Although paternal-antigen specific Treg cells have not been identified in humans, recent studies suggest that antigen-specific Treg cells exist and expand at the feto-maternal interface in humans. Studies have also revealed that reduction of decidual functional Treg cells occurs during miscarriage with normal fetal chromosomal content, whereas insufficient clonal expansion of decidual Treg cells is observed in preeclampsia. In this review, we will discuss the recent advances in the investigation of mechanisms underlying Treg cell-dependent maintenance of feto-maternal tolerance.
半同种异体胎儿不会被母体免疫系统排斥,因为 CD4CD25FoxP3 调节性 T(Treg)细胞诱导的胎母耐受在妊娠期间建立。在妊娠期间,父系抗原特异性 Treg 细胞会积累,而精液诱导在扩增鼠模型中的父系抗原特异性 Treg 细胞中发挥重要作用。尽管尚未在人类中鉴定出父系抗原特异性 Treg 细胞,但最近的研究表明,抗原特异性 Treg 细胞在人类胎母界面存在并扩增。研究还表明,在正常胎儿染色体含量的自然流产中,蜕膜功能 Treg 细胞减少,而子痫前期中,蜕膜 Treg 细胞的克隆扩增不足。在这篇综述中,我们将讨论关于 Treg 细胞依赖性维持胎母耐受的机制的最新进展。