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dc.contributor.authorGanal, Stephanie C
dc.contributor.authorSanos, Stephanie L
dc.contributor.authorKallfass, Carsten
dc.contributor.authorOberle, Karin
dc.contributor.authorJohner, Caroline
dc.contributor.authorKirschning, Carsten
dc.contributor.authorLienenklaus, Stefan
dc.contributor.authorWeiss, Siegfried
dc.contributor.authorStaeheli, Peter
dc.contributor.authorAichele, Peter
dc.contributor.authorDiefenbach, Andreas
dc.date.accessioned2012-09-17T12:35:00Z
dc.date.available2012-09-17T12:35:00Z
dc.date.issued2012-07-27
dc.identifier.citationPriming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. 2012, 37 (1):171-86 Immunityen_GB
dc.identifier.issn1097-4180
dc.identifier.pmid22749822
dc.identifier.doi10.1016/j.immuni.2012.05.020
dc.identifier.urihttp://hdl.handle.net/10033/244298
dc.description.abstractMononuclear phagocytes are an important component of an innate immune system perceived as a system ready to react upon encounter of pathogens. Here, we show that in response to microbial stimulation, mononuclear phagocytes residing in nonmucosal lymphoid organs of germ-free mice failed to induce expression of a set of inflammatory response genes, including those encoding the various type I interferons (IFN-I). Consequently, NK cell priming and antiviral immunity were severely compromised. Whereas pattern recognition receptor signaling and nuclear translocation of the transcription factors NF-κB and IRF3 were normal in mononuclear phagocytes of germ-free mice, binding to their respective cytokine promoters was impaired, which correlated with the absence of activating histone marks. Our data reveal a previously unrecognized role for postnatally colonizing microbiota in the introduction of chromatin level changes in the mononuclear phagocyte system, thereby poising expression of central inflammatory genes to initiate a powerful systemic immune response during viral infection.
dc.language.isoenen
dc.rightsArchived with thanks to Immunityen_GB
dc.titlePriming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota.en
dc.typeArticleen
dc.contributor.departmentIMMH, Institute of Medical Microbiology and Hygiene, University of Freiburg, Hermann-Herder-Strasse 11, 79104 Freiburg, Germany; Spemann Graduate School of Biology and Medicine, Albertstrasse 19A, 79104 Freiburg, Germany.en_GB
dc.identifier.journalImmunityen_GB
refterms.dateFOA2018-06-13T01:03:56Z
html.description.abstractMononuclear phagocytes are an important component of an innate immune system perceived as a system ready to react upon encounter of pathogens. Here, we show that in response to microbial stimulation, mononuclear phagocytes residing in nonmucosal lymphoid organs of germ-free mice failed to induce expression of a set of inflammatory response genes, including those encoding the various type I interferons (IFN-I). Consequently, NK cell priming and antiviral immunity were severely compromised. Whereas pattern recognition receptor signaling and nuclear translocation of the transcription factors NF-κB and IRF3 were normal in mononuclear phagocytes of germ-free mice, binding to their respective cytokine promoters was impaired, which correlated with the absence of activating histone marks. Our data reveal a previously unrecognized role for postnatally colonizing microbiota in the introduction of chromatin level changes in the mononuclear phagocyte system, thereby poising expression of central inflammatory genes to initiate a powerful systemic immune response during viral infection.


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