Innate Immunity to Virus Infection
By O. Takeuchi, Shizuo Akira. Immunological Reviews, 2009
1,241 citations recorded by the source corpus.
Summary: The innate immune system is essential for the initial detection of invading viruses and subsequent activation of adaptive immunity. Three classes of receptors, designated retinoic acid‐inducible gene I (RIG‐I)‐like receptors (RLRs), Toll‐like receptors (TLRs), and nucleotide oligomerization domain (NOD)‐like receptors (NLRs), sense viral components, such as double‐stranded RNA (dsRNA), single‐stranded RNA, and DNA. RLRs and TLRs play essential roles in the production of type I interferons (IFNs) and proinflammatory cytokines in cell type‐specific manners. While the RLRs play essential roles in the recognition of RNA viruses in various cells, plasmacytoid dendritic cells utilize TLRs for detecting virus invasion. NLRs play a role in the production of mature interleukin‐1β to dsRNA stimulation. Activation of innate immune cells is critical for mounting adaptive immune responses. In this review, we discuss recent advances in our understanding of the mechanisms of viral RNA recognition by these different types of receptors and its relation to acquired immune responses.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/88f4e3c671df9b8938bca16f1b45b4a11df2bd85
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Citations in the corpus
- Structural and functional insights into pattern recognition by the innate immune receptor RIG-I (2010, background): “Its members include RIG-I, melanoma differentiation–associated gene 5 (MDA5) and laboratory of genetics and physiology-2 (LGP2) receptor”
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- Plasmacytoid Dendritic Cells: Recent Progress and Open Questions (2011, background): “Given the recent extensive reviews on the subject (3, 65), we briefly discuss only several factors contributing to the unique pDC functionality.”
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- A physical and regulatory map of host-influenza interactions reveals pathways in H1N1 infection. (2009, background): “Upon infection by influenza, host cells detect viral RNA through pathogen sensors, such as RIG-I, and induce type I interferons (IFNs) and an antiviral program that is common to many RNA C viruses (Figure 1A) (Takeuchi and Akira, 2009).”
- Ribose 2′-O-methylation provides a molecular signature for the distinction of self and non-self mRNA dependent on the RNA sensor Mda5 (2011, positive): “The activated IFNAR triggers a signaling pathway consisting of the kinase Jak and STAT transcription factors, inducing the expression of a large array of interferon-stimulated genes encoding molecules with antiviral activity, thus establishing the so-called 'host cell antiviral state”
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