期刊
IMMUNITY
卷 37, 期 1, 页码 171-186出版社
CELL PRESS
DOI: 10.1016/j.immuni.2012.05.020
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类别
资金
- Deutsche Forschungsgemeinschaft (SGBM)
- Deutsche Forschungsgemeinschaft [SFB992]
- Bundesministerium fur Bildung und Forschung
- Centrum fur Chronische Immundefizienz
- Boehringer Ingelheim Fonds
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-kappa B 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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