RNA degradation in antiviral immunity and autoimmunity.
Bottom Line: Recent findings have revealed a role for NMD in targeting viral RNA molecules, thereby restricting virus infection.Interestingly, NMD is also linked to immune responses at another level: mutations affecting the NMD or RNA exosome machineries cause chronic activation of defence programmes, resulting in autoimmune phenotypes.Here we place these observations in the context of other links between innate antiviral immunity and type I interferon mediated disease and examine two models: one in which expression or function of pathogen sensors is perturbed and one wherein host-derived RNA molecules with a propensity to activate such sensors accumulate.
Affiliation: Medical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.Show MeSH
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Mentions: Nucleic acids are potent activators of the innate immune response in mammals and numerous specialised nucleic acid-sensing PRRs and their downstream signalling cascades have been identified  (Figure 2). The detection of viral and bacterial nucleic acids triggers a powerful innate immune response that is characterised by the production of type I interferons (IFNs). Type I IFNs signal via the type I interferon receptor to activate transcription of hundreds of ISGs, many of which restrict virus infection . This thereby induces an antiviral state both in the infected cell as well as in the surrounding tissue microenvironment. The type I IFN-induced antiviral state prevents virus replication and spread and constitutes an important barrier to infection; this is evident, for example, from the fact almost every mammalian virus counteracts and/or evades the IFN response [52,53]. Moreover, type I IFNs facilitate cell-mediated innate and adaptive immune responses [54,55]. Type I IFNs are therefore crucial to successful immunity against virus infection.
Affiliation: Medical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.