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IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise

Abstract : Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in Ifitm-deleted mice. Thus, excessive levels of IFITMs may mediate the pregnancy complications observed during congenital infections and other IFN-induced pathologies.
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Julian Buchrieser, Severine S. Degrelle, Thérèse Couderc, Quentin Nevers, Olivier Disson, et al.. IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise. Science, American Association for the Advancement of Science (AAAS), 2019, 365 (6449), pp.176-180. ⟨10.1126/science.aaw7733⟩. ⟨pasteur-02454300⟩



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