胎盘
免疫学
炎症
医学
子宫内
生物
胎儿
怀孕
遗传学
作者
Alfred T. Harding,Marisa Goff,Heather M. Froggatt,Jean K. Lim,Nicholas S. Heaton
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2021-01-15
卷期号:371 (6526): 271-276
被引量:34
标识
DOI:10.1126/science.aba9001
摘要
GPER1 in utero to the rescue! Several common pathogens, including influenza A virus (IAV), can activate systemic type I interferon (IFN) signaling during pregnancy. Such infections would be expected to cause birth defects and fetal mortality, but maternal IAV infections rarely produce such effects, suggesting the presence of a protective mechanism in fetal tissues. Harding et al. used a CRISPR screen to uncover IFN regulators that can mediate differential IFN control across tissues in human cell lines. They found that G protein–coupled estrogen receptor 1 (GPER1), which is expressed in fetal tissues, acts as a protective suppressor of IFN responses in the placenta during maternal infection. In a mouse model, pharmacological activation of GPER1 shielded fetuses from maternal inflammation. Activation of GPER1 might be promising therapeutically to protect the fetus from both maternal and fetal infections. Science , this issue p. 271
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