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
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
收藏
页码:1073 / U49
页数:9
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