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      Innate recognition of non-self nucleic acids

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      Author(s): 1 , , 2 ,
      Publication date (Electronic):
      Journal: Genome Biology
      Publisher: BioMed Central

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          Abstract

          A variety of innate immune system receptors recognize and respond to the nucleic acids of invading pathogens.

          Abstract

          The immune system has evolved a plethora of innate receptors that detect microbial DNA and RNA, including Toll-like receptors in the endosomal compartment and RIG-I-like receptors and Nod-like receptors in the cytosol. Here we discuss the recognition of and responses to non-self nucleic acids via these receptors as well as their involvement in autoimmune diseases.

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          Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

          Sandra S. Diebold, Tsuneyasu Kaisho, Hiroaki Hemmi … (2004)
          Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-alpha in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory cytokines. These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.
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            Recognition of microorganisms and activation of the immune response.

            Ruslan Medzhitov (2007)
            The mammalian immune system has innate and adaptive components, which cooperate to protect the host against microbial infections. The innate immune system consists of functionally distinct 'modules' that evolved to provide different forms of protection against pathogens. It senses pathogens through pattern-recognition receptors, which trigger the activation of antimicrobial defences and stimulate the adaptive immune response. The adaptive immune system, in turn, activates innate effector mechanisms in an antigen-specific manner. The connections between the various immune components are not fully understood, but recent progress brings us closer to an integrated view of the immune system and its function in host defence.
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              RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates.

              Andreas Pichlmair, Oliver Schulz, Choon Ping Tan … (2006)
              Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Biol
                Title: Genome Biology
                Publisher: BioMed Central
                ISSN (Print): 1465-6906
                ISSN (Electronic): 1465-6914
                Publication date (Print): 2008
                Publication date (Electronic): 10 March 2008
                Volume: 9
                Issue: 3
                Page: 211
                Affiliations
                [1 ]Department of Immunology, St Jude Children's Research Hospital, Memphis, TN 38105, USA
                [2 ]Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
                Article
                Publisher ID: gb-2008-9-3-211
                DOI: 10.1186/gb-2008-9-3-211
                PMC ID: 2397494
                PubMed ID: 18341708
                SO-VID: 4b72e560-ffca-49b3-b1c7-68b8f177ef04
                Copyright © Copyright © 2008 BioMed Central Ltd
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                Subject: Review

                ScienceOpen disciplines: Genetics
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                ScienceOpen disciplines: Genetics

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