期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 284, 期 44, 页码 30058-30066出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M109.018283
关键词
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资金
- National Institutes of Health [AI 058211, HL 55413, 5T32 AI07525, 5T32 DK007328, AI 059715, AI23549]
- Austrian Science Foundation [P20522-B05]
- Austrian Science Fund (FWF) [P20522] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [F 2803] Funding Source: researchfish
Legionella pneumophila remains an important opportunistic pathogen of human macrophages. Its more limited ability to replicate in murine macrophages has been attributed to redundant innate sensor systems that detect and effectively respond to this infection. The current studies evaluate the role of one of these innate response systems, the type I interferon (IFN-I) autocrine loop. The ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3, but not NF-kappa B. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila. Surprisingly, this suppression is mediated by a pathway that is independent of Stat1, Stat2, Stat3, but correlates with the polarization of macrophages toward the M1 or classically activated phenotype.
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