Interferon-inducible effector mechanisms in cell-autonomous immunity

被引:488
作者
MacMicking, John D. [1 ]
机构
[1] Yale Univ, Sch Med, Boyer Ctr Mol Med, Sect Microbial Pathogenesis, New Haven, CT 06510 USA
基金
美国国家卫生研究院;
关键词
GUANYLATE-BINDING PROTEIN-1; STOMATITIS-VIRUS INFECTION; IRG RESISTANCE GTPASES; NITRIC-OXIDE SYNTHASE; TOXOPLASMA-GONDII; GAMMA-INTERFERON; HOST-RESISTANCE; MYCOBACTERIUM-TUBERCULOSIS; LISTERIA-MONOCYTOGENES; CHLAMYDIA-TRACHOMATIS;
D O I
10.1038/nri3210
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Interferons (IFNs) induce the expression of hundreds of genes as part of an elaborate antimicrobial programme designed to combat infection in all nucleated cells-a process termed cell-autonomous immunity. As described in this Review, recent genomic and subgenomic analyses have begun to assign functional properties to novel IFN-inducible effector proteins that restrict bacteria, protozoa and viruses in different subcellular compartments and at different stages of the pathogen life cycle. Several newly described host defence factors also participate in canonical oxidative and autophagic pathways by spatially coordinating their activities to enhance microbial killing. Together, these IFN-induced effector networks help to confer vertebrate host resistance to a vast and complex microbial world.
引用
收藏
页码:367 / 382
页数:16
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