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J Exp Med. 2016 Jan 11;213(1):1-13. doi: 10.1084/jem.20151531. Epub 2015 Dec 28.

Ubiquitin in the activation and attenuation of innate antiviral immunity.

Author information

1
Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
2
Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia dixit@gene.com natalie.borg@monash.edu.
3
Department of Physiological Chemistry, Genentech, Inc., South San Francisco, CA 94080 dixit@gene.com natalie.borg@monash.edu.

Abstract

Viral infection activates danger signals that are transmitted via the retinoic acid-inducible gene 1-like receptor (RLR), nucleotide-binding oligomerization domain-like receptor (NLR), and Toll-like receptor (TLR) protein signaling cascades. This places host cells in an antiviral posture by up-regulating antiviral cytokines including type-I interferon (IFN-I). Ubiquitin modifications and cross-talk between proteins within these signaling cascades potentiate IFN-I expression, and inversely, a growing number of viruses are found to weaponize the ubiquitin modification system to suppress IFN-I. Here we review how host- and virus-directed ubiquitin modification of proteins in the RLR, NLR, and TLR antiviral signaling cascades modulate IFN-I expression.

PMID:
26712804
PMCID:
PMC4710203
DOI:
10.1084/jem.20151531
[Indexed for MEDLINE]
Free PMC Article

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