Journal
NATURE IMMUNOLOGY
Volume 10, Issue 10, Pages 1073-U49Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1782
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Funding
- National Institutes of Health [P30 CA54174, P30 AG013319, P01AG19316, AI069062, CA129246, T32-DE14318, AI067716]
- American Lung Association [AI067716, RG-49629-N]
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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.
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