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Rad50-CARD9 interactions link cytosolic DNA sensing to IL-1β production.
Nat. Immunol. 15, 538-545 (2014)
Double-stranded DNA (dsDNA) in the cytoplasm triggers the production of interleukin 1β (IL-1β) as an antiviral host response, and deregulation of the pathways involved can promote inflammatory disease. Here we report a direct cytosolic interaction between the DNA-damage sensor Rad50 and the innate immune system adaptor CARD9. Transfection of dendritic cells with dsDNA or infection of dendritic cells with a DNA virus induced the formation of dsDNA-Rad50-CARD9 signaling complexes for activation of the transcription factor NF-κB and the generation of pro-IL-1β. Primary cells conditionally deficient in Rad50 or lacking CARD9 consequently exhibited defective DNA-induced production of IL-1β, and Card9(-/-) mice had impaired inflammatory responses after infection with a DNA virus in vivo. Our results define a cytosolic DNA-recognition pathway for inflammation and a physical and functional connection between a conserved DNA-damage sensor and the innate immune response to pathogens.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Vaccinia Virus Ankara; Adapter Protein Card9; Cyclic Gmp-amp; Innate Immunity; I Interferon; Aim2 Inflammasome; Damage Response; Dendritic Cells; Rig-i; Receptors
ISSN (print) / ISBN
1529-2908
e-ISSN
1529-2916
Zeitschrift
Nature Immunology
Quellenangaben
Band: 15,
Heft: 6,
Seiten: 538-545
Verlag
Nature Publishing Group
Verlagsort
New York
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Virology (VIRO)