<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ben-Yehuda H</submitter><funding>European Research Council</funding><funding>Israel Science Foundation (ISF)</funding><pagination>1050-1067</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7192855</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(5)</volume><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</pubmed_abstract><journal>Molecular psychiatry</journal><pubmed_title>Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress.</pubmed_title><pmcid>PMC7192855</pmcid><funding_grant_id>1354/15</funding_grant_id><funding_grant_id>741744</funding_grant_id><funding_grant_id>991/16</funding_grant_id><pubmed_authors>Ben-Yehuda H</pubmed_authors><pubmed_authors>Prinz M</pubmed_authors><pubmed_authors>Matcovitch-Natan O</pubmed_authors><pubmed_authors>Kertser A</pubmed_authors><pubmed_authors>Schwartz M</pubmed_authors><pubmed_authors>Amit I</pubmed_authors><pubmed_authors>Spinrad A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring accompanied by increased sensitivity to stress.</name><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</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-22T06:28:13.669Z</modification><creation>2020-05-22T19:13:57Z</creation></dates><accession>S-EPMC7192855</accession><cross_references><pubmed>31772304</pubmed><doi>10.1038/s41380-019-0604-0</doi></cross_references></HashMap>