Activation of innate immune antiviral responses by Nod2

被引：582

作者：

Sabbah, Ahmed ^{[1
]}

Chang, Te Hung ^{[1
]}

Harnack, Rosalinda ^{[1
]}

Frohlich, Victoria ^{[2
]}

Tominaga, Kaoru ^{[2
,3
]}

Dube, Peter H. ^{[1
]}

Xiang, Yan ^{[1
]}

Bose, Santanu ^{[1
]}

机构：

[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA

[2] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA

[3] Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA

来源：

NATURE IMMUNOLOGY | 2009年 / 10卷 / 10期

基金：

美国国家卫生研究院;

关键词：

RESPIRATORY SYNCYTIAL VIRUS; TOLL-LIKE RECEPTORS; NF-KAPPA-B; RIG-I; EPITHELIAL-CELLS; RNA VIRUSES; PARAINFLUENZA VIRUS; VIRAL-INFECTION; INFLUENZA-VIRUS; HOST-DEFENSE;

D O I：

10.1038/ni.1782

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs) and RIG-like helicase (RLH) receptors, are involved in innate immune antiviral responses. Here we show that nucleotide-binding oligomerization domain 2 (Nod2) can also function as a cytoplasmic viral PRR by triggering activation of interferon-regulatory factor 3 (IRF3) and production of interferon-beta (IFN-beta). After recognition of a viral ssRNA genome, Nod2 used the adaptor protein MAVS to activate IRF3. Nod2-deficient mice failed to produce interferon efficiently and showed enhanced susceptibility to virus-induced pathogenesis. Thus, the function of Nod2 as a viral PRR highlights the important function of Nod2 in host antiviral defense mechanisms.

引用

页码：1073 / U49

页数：9

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