<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Stegemann-Koniszewski S</submitter><funding>Helmholtz-Gemeinschaft</funding><funding>Deutsche Forschungsgemeinschaft</funding><pagination>e00276-16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4959657</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(3)</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>Influenza A virus (IAV) periodically causes substantial morbidity and mortality in the human population. In the lower lung, the primary targets for IAV replication are type II alveolar epithelial cells (AECII), which are increasingly recognized for their immunological potential. So far, little is known about their reaction to IAV and their contribution to respiratory antiviral immunity in vivo Therefore, we characterized the AECII response during early IAV infection by analyzing transcriptional regulation in cells sorted from the lungs of infected mice. We detected rapid and extensive regulation of gene expression in AECII following in vivo IAV infection. The comparison to transcriptional regulation in lung tissue revealed a strong contribution of AECII to the respirator</pubmed_abstract><journal>mBio</journal><pubmed_title>Alveolar Type II Epithelial Cells Contribute to the Anti-Influenza A Virus Response in the Lung by Integrating Pathogen- and Microenvironment-Derived Signals.</pubmed_title><pmcid>PMC4959657</pmcid><funding_grant_id>W2/W3-029</funding_grant_id><funding_grant_id>BR2221/1-1</funding_grant_id><funding_grant_id>GU769/5-1</funding_grant_id><pubmed_authors>Jeron A</pubmed_authors><pubmed_authors>Stegemann-Koniszewski S</pubmed_authors><pubmed_authors>Gereke M</pubmed_authors><pubmed_authors>Geffers R</pubmed_authors><pubmed_authors>Bruder D</pubmed_authors><pubmed_authors>Gunzer M</pubmed_authors><pubmed_authors>Kroger A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Alveolar Type II Epithelial Cells Contribute to the Anti-Influenza A Virus Response in the Lung by Integrating Pathogen- and Microenvironment-Derived Signals.</name><description>&lt;h4>Unlabelled&lt;/h4>Influenza A virus (IAV) periodically causes substantial morbidity and mortality in the human population. In the lower lung, the primary targets for IAV replication are type II alveolar epithelial cells (AECII), which are increasingly recognized for their immunological potential. So far, little is known about their reaction to IAV and their contribution to respiratory antiviral immunity in vivo Therefore, we characterized the AECII response during early IAV infection by analyzing transcriptional regulation in cells sorted from the lungs of infected mice. We detected rapid and extensive regulation of gene expression in AECII following in vivo IAV infection. The comparison to transcriptional regulation in lung tissue revealed a strong contribution of AECII to the respirator</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 May</publication><modification>2026-04-17T17:04:15.499Z</modification><creation>2019-03-27T02:19:05Z</creation></dates><accession>S-EPMC4959657</accession><cross_references><pubmed>27143386</pubmed><doi>10.1128/mBio.00276-16</doi></cross_references></HashMap>