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Immunity
Article
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Immunity
Article . 2005
License: Elsevier Non-Commercial
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Immunity
Article . 2005 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Immunity
Article . 2005
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Cell Type-Specific Involvement of RIG-I in Antiviral Response

Authors: Kato, Hiroki; Sato, Shintaro; Yoneyama, Mitsutoshi; Yamamoto, Masahiro; Uematsu, Satoshi; Matsui, Kosuke; Tsujimura, Tohru; +4 Authors

Cell Type-Specific Involvement of RIG-I in Antiviral Response

Abstract

Toll-like receptors (TLRs) play an important role in antiviral response by recognizing viral components. Recently, a RNA helicase, RIG-I, was also suggested to recognize viral double-stranded RNA. However, how these molecules contribute to viral recognition in vivo is poorly understood. We show by gene targeting that RIG-I is essential for induction of type I interferons (IFNs) after infection with RNA viruses in fibroblasts and conventional dendritic cells (DCs). RIG-I induces type I IFNs by activating IRF3 via IkappaB kinase-related kinases. In contrast, plasmacytoid DCs, which produce large amounts of IFN-alpha, use the TLR system rather than RIG-I for viral detection. Taken together, RIG-I and the TLR system exert antiviral responses in a cell type-specific manner.

Keywords

Newcastle Disease, Immunology, Newcastle disease virus, Receptors, Cell Surface, Protein Serine-Threonine Kinases, DEAD-box RNA Helicases, Mice, RNA Virus Infections, Immunology and Allergy, Animals, Membrane Glycoproteins, Interferon-alpha, Dendritic Cells, Fibroblasts, I-kappa B Kinase, DNA-Binding Proteins, Infectious Diseases, Gene Targeting, Interferon Type I, DEAD Box Protein 58, Interferon Regulatory Factor-3, RNA Helicases, Signal Transduction

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
1K
Top 0.1%
Top 0.1%
Top 0.01%
hybrid