Viral Infections Activate Types I and III Interferon Genes through a Common Mechanism
Viral infections trigger innate immune responses, including the production of type I interferons (IFN-α and -β) and other proinflammatory cytokines. Novel antiviral cytokines IFN-λ1, IFN-λ2, and IFN-λ3 are classified as type III IFNs and have evolved independently of type I IFNs. Type III IFN genes...
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| Veröffentlicht in: | The Journal of biological chemistry 2007-03, Vol.282 (10), p.7576-7581 |
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| container_title | The Journal of biological chemistry |
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| creator | Onoguchi, Kazuhide Yoneyama, Mitsutoshi Takemura, Azumi Akira, Shizuo Taniguchi, Tadatsugu Namiki, Hideo Fujita, Takashi |
| description | Viral infections trigger innate immune responses, including the production of type I interferons (IFN-α and -β) and other proinflammatory cytokines. Novel antiviral cytokines IFN-λ1, IFN-λ2, and IFN-λ3 are classified as type III IFNs and have evolved independently of type I IFNs. Type III IFN genes are regulated at the level of transcription and induced by viral infection. Although the regulatory mechanism of type I IFNs is well elucidated, the expression mechanism of IFN-λs is not well understood. Here, we analyzed the mechanism by which IFN-λ gene expression is induced by viral infections. Loss- and gain-of-function experiments revealed the involvement of RIG-I (retinoic acid-inducible gene I), IPS-1, TBK1, and interferon regulatory factor-3, key regulators of the virus-induced activation of type I IFN genes. Consistent with this, a search for the cis-regulatory element of the human ifnλ1 revealed a cluster of interferon regulatory factor-binding sites and a NF-κB-binding site. Functional analysis demonstrated that all of these sites are essential for gene activation by the virus. These results strongly suggest that types I and III IFN genes are regulated by a common mechanism. |
| doi_str_mv | 10.1074/jbc.M608618200 |
| format | Article |
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Novel antiviral cytokines IFN-λ1, IFN-λ2, and IFN-λ3 are classified as type III IFNs and have evolved independently of type I IFNs. Type III IFN genes are regulated at the level of transcription and induced by viral infection. Although the regulatory mechanism of type I IFNs is well elucidated, the expression mechanism of IFN-λs is not well understood. Here, we analyzed the mechanism by which IFN-λ gene expression is induced by viral infections. Loss- and gain-of-function experiments revealed the involvement of RIG-I (retinoic acid-inducible gene I), IPS-1, TBK1, and interferon regulatory factor-3, key regulators of the virus-induced activation of type I IFN genes. Consistent with this, a search for the cis-regulatory element of the human ifnλ1 revealed a cluster of interferon regulatory factor-binding sites and a NF-κB-binding site. Functional analysis demonstrated that all of these sites are essential for gene activation by the virus. 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| subjects | Adaptor Proteins, Signal Transducing - physiology Animals Binding Sites Cells, Cultured Cytokines - genetics DEAD Box Protein 58 DEAD-box RNA Helicases - physiology Gene Expression Regulation Humans Interferon Regulatory Factor-3 - physiology Interferon Type I - genetics Interferons Interleukins - genetics Mice NF-kappa B - metabolism Protein Serine-Threonine Kinases - physiology Receptors, Immunologic Signal Transduction Transcription Initiation Site Transcriptional Activation Virus Diseases - immunology |
| title | Viral Infections Activate Types I and III Interferon Genes through a Common Mechanism |
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