Activation of innate immune antiviral response by NOD2

By A. Sabbah, T. Chang, Rosalinda Harnack, Victoria C. Frohlich, Kaoru Tominaga, P. Dube, Y. Xiang, Santanu Bose. Nature Immunology, 2009

775 citations recorded by the source corpus.

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-β (IFN-β). 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.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/3873633da9de37b56a770a1298d840f8d95418ae

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Citations in the corpus

Genetics and pathogenesis of inflammatory bowel disease (2011, background): “Furthermore, NOD2 can participate in distinct MDP-independent pathways such as regulation of the T-cell response and the type I IFN response to single-stranded RNA (ssRNA) stimulation, indicating that gut microbial ssRNAs may exist and have immunomodulatory propertie”
Into the Eye of the Cytokine Storm (2012, background): “As discussed above, there are several classes of cellular PRRs that activate and modulate innate immunity during infection, the specificity of which is determined by the recognized microbial motif, including TLRs that engage LPS, molecules derived from protozoan parasites, and viral RNA products (11”
Virus-Plus-Susceptibility Gene Interaction Determines Crohn’s Disease Gene Atg16L1 Phenotypes in Intestine (2010, background): “Interestingly, the Crohn’s disease associated gene NOD2 may recognize viral RNA in addition to bacterial peptidoglycan (Sabbah et al., 2009; Shapira et al., 2009), raising the possibility that a viral infection can interact with multiple susceptibility genes.”
A physical and regulatory map of host-influenza interactions reveals pathways in H1N1 infection. (2009, background): “…PRKRA, a known regulator of PKR (in P20) and TRAF6 (in P13), known essential regulators of PR8 replication such as NXF1 (P17) and PGD (P17) (Hao et al., 2008; Satterly et al., 2007), and inflammasome-associated components (NOD2 and NLRP9, P18), consistent with recent findings (Sabbah et al., 2009).”
Pattern recognition receptors and inflammation. (2010, background): “In addition to bacteria, a recent study found that the expression of NOD2 is involved in 5 0 -triphosphate RNA-induced type I IFN production and host defense against respiratory syncytial virus infection (Sabbah et al., 2009).”