Valencia-Ortega Jorge, Saucedo Renata, Peña-Cano María I, Hernández-Valencia Marcelino, Cruz-Durán José G
Endocrine Research Unit, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Faculty of Chemistry, Universidad Autónoma del Estado de México, Toluca, Mexico.
J Obstet Gynaecol Res. 2020 Jul;46(7):1067-1076. doi: 10.1111/jog.14309. Epub 2020 May 19.
The objective of this review is to describe the immunological mechanisms which facilitate maternal tolerance at the maternal-placental interface, and to discuss how these mechanisms are disrupted in pre-eclampsia.
A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the immunological mechanisms which facilitate maternal tolerance in healthy pregnancy and pre-eclampsia are presented in this article.
The maternal-placental interface is the site where the immune tolerance begins and develops. Within the innate immunity, natural killer cells, macrophages and dendritic cells play a pivotal role in tolerance through regulation of inflammation. On the other hand, within the adaptive immunity, the correct increase of regulatory T cells is crucial for ensuring immune tolerance toward placental cells. Disturbances in maternal tolerance can lead to the appearance of pregnancy complications such as pre-eclampsia, which has a considerable impact on perinatal morbidity and mortality.
Our partial knowledge of immunological mechanisms involved in tolerance at the maternal-placental interface indicates that pre-eclampsia is characterized by alterations of this maternal immune tolerance, which could represent the origin of the disease.
本综述的目的是描述在母胎 - 胎盘界面促进母体免疫耐受的免疫机制，并讨论这些机制在子痫前期是如何被破坏的。
基于对PubMed上可用论文的分析进行文献综述。本文介绍了关于在正常妊娠和子痫前期促进母体免疫耐受的免疫机制的最重要和相关的研究。
母胎 - 胎盘界面是免疫耐受开始和发展的部位。在固有免疫中，自然杀伤细胞、巨噬细胞和树突状细胞通过调节炎症在耐受中起关键作用。另一方面，在适应性免疫中，调节性T细胞的正确增加对于确保对胎盘细胞的免疫耐受至关重要。母体耐受的紊乱可导致如子痫前期等妊娠并发症的出现，这对围产期发病率和死亡率有相当大的影响。
我们对母胎 - 胎盘界面耐受所涉及的免疫机制的部分了解表明，子痫前期的特征是这种母体免疫耐受的改变，这可能是该疾病的起源。
