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Adenosine-to-inosine editing of endogenous Z-form RNA by the deaminase ADAR1 prevents spontaneous MAVS-dependent type I interferon responses

Authors
  • Tang, Qiannan1
  • Rigby, Rachel E.1
  • Young, George R.2
  • Hvidt, Astrid Korning1
  • Davis, Tanja1
  • Tan, Tiong Kit1
  • Bridgeman, Anne1
  • Townsend, Alain R.1, 3
  • Kassiotis, George4, 5
  • Rehwinkel, Jan1
  • 1 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
  • 2 Bioinformatics and Biostatistics STP, The Francis Crick Institute, London, NW1 1AT, UK
  • 3 Centre for Translational Immunology, Chinese Academy of Medical Sciences Oxford Institute, University of Oxford, Oxford, OX3 7FZ, UK
  • 4 Retroviral Immunology, The Francis Crick Institute, London, NW 1AT, UK
  • 5 Department of Infectious Disease, Faculty of Medicine, Imperial College London, London, W2 1NY, UK
Type
Published Article
Journal
Immunity
Publication Date
Sep 14, 2021
Volume
54
Issue
9
Pages
1961–1975
Identifiers
DOI: 10.1016/j.immuni.2021.08.011
PMID: 34525337
PMCID: PMC8459395
Source
PubMed Central
Keywords
Disciplines
  • Article
License
Unknown

Abstract

Nucleic acids can adopt the Z-conformation, an unusual left-handed double helix. Tang et al. show that mutations in the Z-RNA recognition domain of the adenosine deaminase ADAR1 result in spontaneous type I interferon production. Analysis of adenosine-to-inosine changes shows enrichment in transposable elements and suggests that editing by ADAR1 curtails the immunostimulatory potential of endogenous Z-form RNAs, with relevance to autoinflammatory disease in humans.

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