Cell Type-Specific Involvement of RIG-I in Antiviral Response
Open accessAbstract
Toll-like receptors (TLRs) play an important role in antiviral response by recognizing viral components. Recently, a RNA helicase, RIG-I, is also suggested to recognize viral double-stranded RNA. However, how these molecules contribute to viral recognition in vivo is poorly understood. Here we would like to show 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 DC, 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.
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In the absence of RIG-I signaling, mice fail to produce type I IFN in response to vesicular stomatitis virus, Newcastle disease virus, and Sendai virus infection.
“In the absence of RIG-I signaling, mice fail to produce type I IFN in response to vesicular stomatitis virus (VSV), Newcastle disease virus (NDV), and Sendai virus infection (74).”
From Into the Eye of the Cytokine Storm (2012) · cites this paper as [74]
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- Authors
- Kato, H., Sato, S., Yoneyama, M., Yamamoto, M., Uematsu, S., Matsui, K., Tsujimura, T., Takeda, K., Fujita, T., Takeuchi, O., & Akira, S.
- Affiliations
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Japan Science and Technology Agency (JP)
- Tokyo Metropolitan Institute of Medical Science (JP)
- Hyogo Medical University (JP)
- Kyushu University (JP)
- Corresponding author
- Akira, Shizuo
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2005-07
- Volume
- 23
- Issue
- 1
- Pages
- 19-28
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2138677670
- Cited by
- 1,368
- References
- 49
- Citations by year
- 2026: 18 · 2025: 27 · 2024: 31 · 2023: 34 · 2022: 43 · 2021: 41 · 2020: 50 · 2019: 36 · 2018: 49 · 2017: 50 · 2016: 45 · 2015: 41 · 2014: 95 · 2013: 81 · 2012: 68
- FWCI
- 43.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2974 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- RIG-I, RNA helicase, type I interferon, antiviral innate immunity, Toll-like receptors, IRF3 activation, IκB kinase, plasmacytoid dendritic cells, myeloid dendritic cells, fibroblasts, double-stranded RNA sensing, cell type-specific signaling
- MeSH terms
- DEAD Box Protein 58, Animals, Dendritic Cells, DNA-Binding Proteins, Fibroblasts, Interferon Type I, Membrane Glycoproteins, Newcastle Disease, Newcastle disease virus, Receptors, Cell Surface, RNA Virus Infections, Transcription Factors, Signal Transduction, Interferon-alpha, Protein Serine-Threonine Kinases, Gene Targeting, RNA Helicases, Interferon Regulatory Factor-3, Toll-Like Receptors, Mice, I-kappa B Kinase, DEAD-box RNA Helicases
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