期刊
NATURE IMMUNOLOGY
卷 16, 期 1, 页码 67-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3046
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资金
- German Academic Exchange Service
- National Cancer Institute, Center for Cancer Research, of the US National Institutes of Health
- European Molecular Biology Organization [ALTF 48-2008, ALTF 314-2012]
- Austrian Academy of Sciences
- Swiss National Science Foundation [PP00P3_152928]
- Klaus-Tschira Foundation
- Gebert-Ruf Foundation
- Ohio State University Comprehensive Cancer Center
- US National Institutes of Health [R01AI032972, R01AI025032, U19AI100627]
- Swiss Foundation for Medical-Biological Stipends
- Austrian Science Fund [P-25360]
- Austrian Science Fund (FWF) [P 25360] Funding Source: researchfish
- NATIONAL CANCER INSTITUTE [ZICBC011265] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI032972, R01AI025032, U19AI100627] Funding Source: NIH RePORTER
Immune responses are tightly regulated to ensure efficient pathogen clearance while avoiding tissue damage. Here we report that Setdb2 was the only protein lysine methyltransferase induced during infection with influenza virus. Setdb2 expression depended on signaling via type I interferons, and Setdb2 repressed expression of the gene encoding the neutrophil attractant CXCL1 and other genes that are targets of the transcription factor NF-kappa B. This coincided with occupancy by Setdb2 at the Cxcl1 promoter, which in the absence of Setdb2 displayed diminished trimethylation of histone H3 Lys9 (H3K9me3). Mice with a hypomorphic gene-trap construct of Setdb2 exhibited increased infiltration of neutrophils during sterile lung inflammation and were less sensitive to bacterial superinfection after infection with influenza virus. This suggested that a Setdb2-mediated regulatory crosstalk between the type I interferons and NF-kappa B pathways represents an important mechanism for virus-induced susceptibility to bacterial superinfection.
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