合胞滋养细胞
合胞体
胎儿
滋养层
生物
细胞融合
多核
胎盘
内生
细胞生物学
跨膜蛋白
Ⅰ型干扰素
干扰素
合胞滋养细胞
怀孕
免疫学
男科
内分泌学
细胞
医学
遗传学
受体
人类免疫缺陷病毒(HIV)
作者
Julian Buchrieser,Séverine A. Degrelle,Thérèse Couderc,Quentin Nevers,Olivier Disson,Caroline Manet,Daniel A. Donahue,Françoise Porrot,Kenzo-Hugo Hillion,Émeline Perthame,Marlene V. Arroyo,Sylvie Souquère,Katinka Ruigrok,Anne Dupressoír,Thiérry Heidmann,Xavier Montagutelli,Thierry Fournier,Marc Lecuit,Olivier Schwartz
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2019-07-12
卷期号:365 (6449): 176-180
被引量:130
标识
DOI:10.1126/science.aaw7733
摘要
Placenta formation and fetal demise A critical step of placental development is the fusion of trophoblast cells into a multi-nucleated syncytiotrophoblast layer. Trophoblast fusion is mediated by syncytins, encoded by endogenous retrovirus–derived envelope glycoproteins. Buchrieser et al. report that interferon-induced transmembrane (IFITM) proteins inhibit syncytin-mediated syncytiotrophoblast formation, restricting placental development and triggering fetal demise (see the Perspective by Kellam and Weiss). The results provide a molecular explanation for the placental dysfunctions observed in interferon-mediated disorders such as intrauterine growth retardation, TORCH (toxoplasmosis, other, rubella, cytomegalovirus, and herpes) infections, and some forms of preeclampsia. Science , this issue p. 176 ; see also p. 118
科研通智能强力驱动
Strongly Powered by AbleSci AI