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  • Title: NLRP2 negatively regulates antiviral immunity by interacting with TBK1.
    Author: Yang Y, Lang X, Sun S, Gao C, Hu J, Ding S, Li J, Li Y, Wang F, Gong T.
    Journal: Eur J Immunol; 2018 Nov; 48(11):1817-1825. PubMed ID: 30183071.
    Abstract:
    Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are intracellular pattern recognition receptors (PRRs) that regulate a variety of inflammatory and host defense responses. Unlike the well-established NLRs, the roles of NLRP2 are controversial and poorly defined. Here, we report that NLRP2 acts as a negative regulator of TANK-binding kinase 1 (TBK1)-mediated type I interferon (IFN) signaling. Mechanistically, NLRP2 interacted directly with TBK1, and this binding disrupted the interaction of TBK1 and interferon regulatory factor 3 (IRF3), which interfered with TBK1-induced IRF3 phosphorylation. IFNs induce a series of proteins that have well-known antiviral or immune-regulatory functions, and tight control of the IFN signaling cascade is critical for limiting tissue damage and preventing autoimmunity. Our studies indicate that the NLRP2-TBK1 axis may serve as an additional signaling cascade to maintain immune homeostasis in response to viral infection.
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