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dc.contributor.authorUluçkan, Özge 
dc.contributor.authorJimenez Maria, M 
dc.contributor.authorRoediger, Ben
dc.contributor.authorSchnabl, Jakob
dc.contributor.authorDíez-Córdova, Lucía T
dc.contributor.authorTroulé, Kevin
dc.contributor.authorWeninger, Wolfgang
dc.contributor.authorWagner, Erwin Friedrich 
dc.date.accessioned2020-03-25T14:28:18Z
dc.date.available2020-03-25T14:28:18Z
dc.date.issued2019-10-22
dc.identifier.citationCell Rep. 2019 ;29(4):844-859es_ES
dc.identifier.issn22111247es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9331
dc.description.abstractAtopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunBΔep mice, with a large transcriptomic overlap with AD. Additionally, using Rag1-/- mice, we demonstrate that adaptive immune cells are necessary for protection against S. aureus colonization. Prophylactic antibiotics, but not antibiotics after established dysbiosis, reduce IL-17A expression and skin inflammation, examined using Il17a-eGFP reporter mice. Mechanistically, keratinocytes lacking JunB exhibit higher MyD88 levels in vitro and in vivo, previously shown to regulate S. aureus colonization. In conclusion, our data identify JunB as an upstream regulator of microbiota-immune cell interactions and characterize the IL-17A response upon spontaneous dysbiosis.es_ES
dc.description.sponsorshipWe thank the Wagner lab for helpful suggestions and discussion throughout the evolution of this project, specifically Alvaro Ucero, Nuria Gago, and Liliana Mellor. We thank Vanessa Bermeo and Guillermo Medrano for help with animal husbandry and genotyping. O.U. was funded by the ECTS/Amgen Bone Biology Fellowship (2013-2016) and by the Spanish Ministry of Economy and Competitiveness (SAF2012-39670). B.R. and W.W. were funded by a Jesus-Serra visiting scientist grant. E.F.W. was funded by a European Research Council advanced grant (ERC FCK/2008/37).es_ES
dc.language.isoenges_ES
dc.publisherCell Presses_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectAP-1es_ES
dc.subjectJunBes_ES
dc.subjectatopic dermatitises_ES
dc.subjectdysbiosises_ES
dc.subjectmicrobiotaes_ES
dc.subjectskin inflammationes_ES
dc.subjecttype 2 immunityes_ES
dc.titleCutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID31644908es_ES
dc.format.volume29es_ES
dc.format.number4es_ES
dc.format.page844-859.e3es_ES
dc.identifier.doi10.1016/j.celrep.2019.09.042es_ES
dc.contributor.funderMinisterio de Economia y Competitividad (MINECO)
dc.contributor.funderEuropean Research Council
dc.description.peerreviewedes_ES
dc.identifier.e-issn2211-1247es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.celrep.2019.09.042.es_ES
dc.identifier.journalCell reportses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Antiguos CNIOes_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/SAF2012-39670es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional