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Lee, Yeon-Su; Bao, Xiaoyong; Lee, Hwi-Ho; Jang, Jiyoung Joan; Saruuldalai, Enkhjin; Park, Gaeul; Im, Wonkyun Ronny; Park, Jong-Lyul; Kim, Seon-Young; Shin, Sooyong; Jeon, Sung Ho; Kang, Sangmin; Lee, Hyun-Sung; Lee, Ju-Seog; Zhang, Ke; Park, Eun Jung; Kim, In-Hoo; Lee, Yong Sun
International journal of molecular sciences, 02/2021, Letnik: 22, Številka: 4Journal Article
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.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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