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dc.contributor.authorHennig, Thomas
dc.contributor.authorDjakovic, Lara
dc.contributor.authorDölken, Lars
dc.contributor.authorWhisnant, Adam W
dc.date.accessioned2021-10-28T09:07:34Z
dc.date.available2021-10-28T09:07:34Z
dc.date.issued2021-09-14
dc.identifier.citationFront Immunol. 2021 Aug 26;12:705436. doi: 10.3389/fimmu.2021.705436.en_US
dc.identifier.pmid34578417
dc.identifier.doi10.3390/v13091836
dc.identifier.urihttp://hdl.handle.net/10033/623083
dc.description.abstractAutophagy is an evolutionary conserved catabolic pathway that ensures the degradation of intracellular components. The autophagic pathway is regulated by autophagy-related (Atg) proteins that govern formation of double-membraned vesicles called autophagosomes. Autophagy deficiency in regulatory T (Treg) cells leads to increased apoptosis of these cells and to the development of autoimmune disorders, predominantly characterized by intestinal inflammation. Recently, RORγt-expressing Treg cells have been identified as key regulators of gut homeostasis, preventing intestinal immunopathology. To study the role of autophagy in RORγt+ Foxp3+ Treg cells, we generated mice lacking the essential component of the core autophagy machinery Atg5 in Foxp3+ cells. Atg5 deficiency in Treg cells led to a predominant intestinal inflammation. While Atg5-deficient Treg cells were reduced in peripheral lymphoid organs, the intestinal RORγt+ Foxp3+ subpopulation of Treg cells was most severely affected. Our data indicated that autophagy is essential to maintain the intestinal RORγt+ Foxp3+ Treg population, thereby protecting the mice from gut inflammatory disorders.en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectC-terminal domainen_US
dc.subjectRNA polymerase IIen_US
dc.subjectherpes simplex virusen_US
dc.subjecthost shutoffen_US
dc.subjectpolyadenylationen_US
dc.subjectpromoter-proximal pausingen_US
dc.subjectsplicingen_US
dc.subjecttranscriptionen_US
dc.titleA Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery.en_US
dc.typeArticleen_US
dc.identifier.eissn1999-4915
dc.contributor.departmentHIRI, Helmholtz-Institut für RNA-basierte Infektionsforschung, Josef-Shneider Strasse 2, 97080 Würzburg, Germany.en_US
dc.identifier.journalVirusesen_US
dc.source.volume13
dc.source.issue9
refterms.dateFOA2021-10-28T09:07:37Z
dc.source.journaltitleViruses
dc.source.countryInternational
dc.source.countrySwitzerland


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International