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A Toll-like receptor-independent antiviral response induced by double-stranded B-form DNA
被引:628
作者:

Ishii, KJ
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Coban, C
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Kato, H
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Takahashi, K
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Torii, Y
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Takeshita, F
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Ludwig, H
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Sutter, G
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Suzuki, K
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Hemmi, H
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Sato, S
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Yamamoto, M
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Uematsu, S
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Kawai, T
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Takeuchi, O
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan

Akira, S
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机构: Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan
机构:
[1] Osaka Univ, Exploratory Res Adv Technol, Japan Sci & Technol Agcy, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Dept Host Def, Suita, Osaka 5650871, Japan
[3] Osaka Univ, 21 Century COE, Combined Program Microbiol & Immunol, Res Inst Microbial Dis, Suita, Osaka 5650871, Japan
[4] Yokohama City Univ, Grad Sch Med, Dept Mol Biodef Res, Yokohama, Kanagawa 2360004, Japan
[5] Paul Ehrlich Inst, Abt Virol, D-63225 Langen, Germany
[6] Natl Inst Infect Dis, Leprosy Res Ctr, Dept Host Def, Tokyo 1890002, Japan
关键词:
D O I:
10.1038/ni1282
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
The innate immune system recognizes nucleic acids during infection or tissue damage; however, the mechanisms of intracellular recognition of DNA have not been fully elucidated. Here we show that intracellular administration of double-stranded B-form DNA (B-DNA) triggered antiviral responses including production of type I interferons and chemokines independently of Toll-like receptors or the helicase RIG-I. B-DNA activated transcription factor IRF3 and the promoter of the gene encoding interferon-beta through a signaling pathway that required the kinases TBK1 and IKKi, whereas there was substantial activation of transcription factor NF-kappa B independent of both TBK and IKKi. IPS-1, an adaptor molecule linking RIG-I and TBK1, was involved in B-DNA-induced activation of interferon-beta and NF-kappa B. B-DNA signaling by this pathway conferred resistance to viral infection in a way dependent on both TBK1 and IKKi. These results suggest that both TBK1 and IKKi are required for innate immune activation by B-DNA, which might be important in antiviral innate immunity and other DNA-associated immune disorders.
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页码:40 / 48
页数:9
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