Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms14392
Keywords
-
Categories
Funding
- Medical Research Council [MR/K00655X/1]
- British Skin Foundation [6057i]
- Tenovus Scotland [T14/14]
- Biotechnology and Biological Sciences Research Council [BB/J004324/1]
- National Institutes of Health [AI093752]
- Science Foundation Ireland [11/PI/1056]
- Wellcome Trust ISSF grant
- MRC doctoral training program at the University of Dundee
- Biotechnology and Biological Sciences Research Council [BBS/E/D/20002172, BBS/E/D/20241864] Funding Source: researchfish
- Medical Research Council [MR/K00655X/1, 1517730, MR/K00655X/2] Funding Source: researchfish
- BBSRC [BBS/E/D/20241864] Funding Source: UKRI
- MRC [MR/K00655X/1, MR/K00655X/2] Funding Source: UKRI
Ask authors/readers for more resources
Many human cells can sense the presence of exogenous DNA during infection though the cytosolic DNA receptor cyclic GMP-AMP synthase (cGAS), which produces the second messenger cyclic GMP-AMP (cGAMP). Other putative DNA receptors have been described, but whether their functions are redundant, tissue-specific or integrated in the cGAS-cGAMP pathway is unclear. Here we show that interferon-g inducible protein 16 (IFI16) cooperates with cGAS during DNA sensing in human keratinocytes, as both cGAS and IFI16 are required for the full activation of an innate immune response to exogenous DNA and DNA viruses. IFI16 is also required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phosphorylation and translocation. We propose that the two DNA sensors IFI16 and cGAS cooperate to prevent the spurious activation of the type I interferon response.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available