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Open Access Green as soon as Postprint is submitted to ZB.
The signaling adaptor TRAF1 negatively regulates Toll-like receptor signaling and this underlies its role in rheumatic disease.
Nat. Immunol. 18, 26-35 (2017)
TRAF1 is a signaling adaptor known for its role in tumor necrosis factor receptor-induced cell survival. Here we show that monocytes from healthy human subjects with a rheumatoid arthritis–associated single-nucleotide polymorphism (SNP) in the TRAF1 gene express less TRAF1 protein but greater amounts of inflammatory cytokines in response to lipopolysaccharide (LPS). The TRAF1 MATH domain binds directly to three components of the linear ubiquitination (LUBAC) complex, SHARPIN, HOIP and HOIL-1, to interfere with the recruitment and linear ubiquitination of NEMO. This results in decreased NF-κB activation and cytokine production, independently of tumor necrosis factor. Consistent with this, Traf1−/− mice show increased susceptibility to LPS-induced septic shock. These findings reveal an unexpected role for TRAF1 in negatively regulating Toll-like receptor signaling, providing a mechanistic explanation for the increased inflammation seen with a disease-associated TRAF1 SNP.
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21.506
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Autoimmunity; Chronic inflammation; NF-kappaB
Language
english
Publication Year
2017
Prepublished in Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
1529-2908
e-ISSN
1529-2916
Journal
Nature Immunology
Quellenangaben
Volume: 18,
Pages: 26-35
Publisher
Nature Publishing Group
Reviewing status
Peer reviewed
Institute(s)
CF Monoclonal Antibodies (CF-MAB)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501760-001
DOI
10.1038/ni.3618
Erfassungsdatum
2016-12-31