Nc886, a novel suppressor of the type I interferon response upon pathogen intrusion

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Nc886, a novel suppressor of the type I interferon response upon pathogen intrusion
Y S Lee; X Bao; H H Lee; J J Jang; E Saruuldalai; G Park; W R Im; Jong Lyul ParkSeon-Young Kim; S Shin; S H Jeon; S Kang; H S Lee; J S Lee; K Zhang; E J Park; I H Kim; Y S Lee
Bibliographic Citation
International Journal of Molecular Sciences, vol. 22, no. 4, pp. 2003-2003
Publication Year
Interferons (IFNs) are a crucial component in the innate immune response. Especially the IFN-β signaling operates in most cell types and plays a key role in the first line of defense upon pathogen intrusion. The induction of IFN-β should be tightly controlled, because its hyperactivation can lead to tissue damage or autoimmune diseases. Activation of the IFN-β promoter needs Interferon Regulatory Factor 3 (IRF3), together with Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Activator Protein 1 (AP-1). Here we report that a human noncoding RNA, nc886, is a novel suppressor for the IFN-β signaling and inflammation. Upon treatment with several pathogen-associated molecular patterns and viruses, nc886 suppresses the activation of IRF3 and also inhibits NF-κB and AP-1 via inhibiting Protein Kinase R (PKR). These events lead to decreased expression of IFN-β and resultantly IFN-stimulated genes. nc886′s role might be to restrict the IFN-β signaling from hyperactivation. Since nc886 expression is regulated by epigenetic and environmental factors, nc886 might explain why innate immune responses to pathogens are variable depending on biological settings.
nc886PathogenInterferonProtein Kinase RInterferon Regulatory Factor 3
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Aging Convergence Research Center > 1. Journal Articles
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