Toll-like receptor 2 on inflammatory monocytes induces type I interferon in response to viral but not bacterial ligands

被引:337
作者
Barbalat, Roman [1 ]
Lau, Laura [1 ]
Locksley, Richard M. [2 ,3 ]
Barton, Gregory M. [1 ]
机构
[1] Univ Calif Berkeley, Div Immunol & Pathogenesis, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Med, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
基金
美国国家卫生研究院;
关键词
CYTOSOLIC DNA; CYTOKINE RESPONSES; DENDRITIC CELLS; MICE LACKING; INNATE; RECOGNITION; ACTIVATION; VIRUS; TLR2; FLAGELLIN;
D O I
10.1038/ni.1792
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Despite the paradigm that the innate immune system uses nucleic acid-specific receptors to detect viruses because of a lack of other conserved features, many viruses are recognized by Toll-like receptor 2 (TLR2) and TLR4. The relevance of this recognition for antiviral immunity remains largely unexplained. Here we report that TLR2 activation by viruses led to the production of type I interferon. TLR2-dependent induction of type I interferon occurred only in response to viral ligands, which indicates that TLR2 is able to discriminate between pathogen classes. We demonstrate that this specialized response was mediated by Ly6C(hi) inflammatory monocytes. Thus, the innate immune system can detect certain non-nucleic acid features of viruses and links this recognition to the induction of specific antiviral genes.
引用
收藏
页码:1200 / U87
页数:9
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