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Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota.
Ganal, Stephanie C Sanos, Stephanie L Kallfass, Carsten Oberle, Karin Johner, Caroline Kirschning, Carsten Lienenklaus, Stefan Weiss, Siegfried Staeheli, Peter Aichele, Peter
Ganal, Stephanie C
Sanos, Stephanie L
Kallfass, Carsten
Oberle, Karin
Johner, Caroline
Kirschning, Carsten
Lienenklaus, Stefan
Weiss, Siegfried
Staeheli, Peter
Aichele, Peter
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2012-07-27
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Mononuclear 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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Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. 2012, 37 (1):171-86 Immunity
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en
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1097-4180
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