Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response
العنوان: | Critical role of TRAF3 in the Toll-like receptor-dependent and -independent antiviral response |
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المؤلفون: | Andrea K. Perry, Arash Shahangian, Genhong Cheng, Supriya K. Saha, Beichu Guo, Brian Zarnegar, Jeannie Q. He, Gagik Oganesyan |
المصدر: | Nature. 439:208-211 |
بيانات النشر: | Springer Science and Business Media LLC, 2005. |
سنة النشر: | 2005 |
مصطلحات موضوعية: | TRAF3, Interferon Regulatory Factor-7, Protein Serine-Threonine Kinases, Biology, Mice, Interferon, Interleukin-1 Receptor-Associated Kinases, medicine, Animals, Toll-like receptor, Multidisciplinary, TNF Receptor-Associated Factor 3, Toll-Like Receptors, Protein kinase R, Immunity, Innate, I-kappa B Kinase, Toll-Like Receptor 3, Mice, Inbred C57BL, Toll-Like Receptor 4, Adaptor Proteins, Vesicular Transport, Phosphotransferases (Alcohol Group Acceptor), Toll-Like Receptor 7, Virus Diseases, TRIF, Toll-Like Receptor 9, Interferon Type I, Immunology, Interferon Regulatory Factor-3, IRF3, medicine.drug |
الوصف: | Type I interferon (IFN) production is a critical component of the innate defence against viral infections. Viral products induce strong type I IFN responses through the activation of Toll-like receptors (TLRs) and intracellular cytoplasmic receptors such as protein kinase R (PKR). Here we demonstrate that cells lacking TRAF3, a member of the TNF receptor-associated factor family, are defective in type I IFN responses activated by several different TLRs. Furthermore, we show that TRAF3 associates with the TLR adaptors TRIF and IRAK1, as well as downstream IRF3/7 kinases TBK1 and IKK-epsilon, suggesting that TRAF3 serves as a critical link between TLR adaptors and downstream regulatory kinases important for IRF activation. In addition to TLR stimulation, we also show that TRAF3-deficient fibroblasts are defective in their type I IFN response to direct infection with vesicular stomatitis virus, indicating that TRAF3 is also an important component of TLR-independent viral recognition pathways. Our data demonstrate that TRAF3 is a major regulator of type I IFN production and the innate antiviral response. |
تدمد: | 1476-4687 0028-0836 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c2b3614dedbff1e1e197991eeb027e5 https://doi.org/10.1038/nature04374 |
حقوق: | CLOSED |
رقم الأكسشن: | edsair.doi.dedup.....8c2b3614dedbff1e1e197991eeb027e5 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 14764687 00280836 |
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