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 Park; Seon-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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