{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ben-Yehuda H"],"funding":["European Research Council","Israel Science Foundation (ISF)"],"pagination":["1050-1067"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7192855"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(5)"],"pubmed_abstract":["Viral infection during pregnancy is often associated with neuropsychiatric conditions. In mice, exposure of pregnant dams to the viral mimetic poly(I:C), serves as a model that simulates such pathology in the offspring, through a process known as Maternal Immune Activation (MIA). To investigate the mechanism of such effect, we hypothesized that maternal upregulation of Type-I interferon (IFN-I), as part of the dam's antiviral response, might contribute to the damage imposed on the offspring. Using mRNA sequencing and flow cytometry analyses we found that poly(I:C) treatment during pregnancy caused reduced expression of genes related to proliferation and cell cycle in the offspring's microglia relative to controls. This was found to be associated with an IFN-I signature in the embryonic yol"],"journal":["Molecular psychiatry"],"pubmed_title":["Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress."],"pmcid":["PMC7192855"],"funding_grant_id":["1354/15","741744","991/16"],"pubmed_authors":["Ben-Yehuda H","Prinz M","Matcovitch-Natan O","Kertser A","Schwartz M","Amit I","Spinrad A"],"additional_accession":[]},"is_claimable":false,"name":"Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress.","description":"Viral infection during pregnancy is often associated with neuropsychiatric conditions. In mice, exposure of pregnant dams to the viral mimetic poly(I:C), serves as a model that simulates such pathology in the offspring, through a process known as Maternal Immune Activation (MIA). To investigate the mechanism of such effect, we hypothesized that maternal upregulation of Type-I interferon (IFN-I), as part of the dam's antiviral response, might contribute to the damage imposed on the offspring. Using mRNA sequencing and flow cytometry analyses we found that poly(I:C) treatment during pregnancy caused reduced expression of genes related to proliferation and cell cycle in the offspring's microglia relative to controls. This was found to be associated with an IFN-I signature in the embryonic yol","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2025-04-22T06:28:13.669Z","creation":"2020-05-22T19:13:57Z"},"accession":"S-EPMC7192855","cross_references":{"pubmed":["31772304"],"doi":["10.1038/s41380-019-0604-0"]}}