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Rad50-CARD9 interactions link cytosolic DNA sensing to IL-1β production.

Abstract：

: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.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Roth S,Rottach A,Lotz-Havla AS,Laux V,Muschaweckh A,Gersting SW,Muntau AC,Hopfner KP,Jin L,Vanness K,Petrini JH,Drexler I,Leonhardt H,Ruland J

doi

10.1038/ni.2888

subject

Has Abstract

pub_date

2014-06-01 00:00:00

pages

538-45

issue

6

eissn

1529-2908

issn

1529-2916

pii

ni.2888

journal_volume

15

pub_type

杂志文章

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