Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota.
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AuthorsGanal, Stephanie C
Sanos, Stephanie L
MetadataShow full item record
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.
CitationPriming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. 2012, 37 (1):171-86 Immunity
AffiliationIMMH, 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.
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