Cited by 1,513Immune Response and InflammationAtherosclerosis and Cardiovascular DiseasesInflammasome and immune disorders

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CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer

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Stewart, Cameron R, Stuart, Lynda M, Wilkinson, Kim, van Gils, Janine M, Deng, Jiusheng, Halle, Annett, Rayner, Katey J, Boyer, Laurent, Zhong, Ruiqin, Frazier, William A, Lacy-Hulbert, Adam, Khoury, Joseph El, Golenbock, Douglas T, Moore, Kathryn J·2010·Nature Immunology

DOI 10.1038/ni.1836PMC PMC2809046

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Abstract

In atherosclerosis and Alzheimer's disease, deposition of the altered self components oxidized low-density lipoprotein (LDL) and amyloid-beta triggers a protracted sterile inflammatory response. Although chronic stimulation of the innate immune system is believed to underlie the pathology of these diseases, the molecular mechanisms of activation remain unclear. Here we show that oxidized LDL and amyloid-beta trigger inflammatory signaling through a heterodimer of Toll-like receptors 4 and 6. Assembly of this newly identified heterodimer is regulated by signals from the scavenger receptor CD36, a common receptor for these disparate ligands. Our results identify CD36-TLR4-TLR6 activation as a common molecular mechanism by which atherogenic lipids and amyloid-beta stimulate sterile inflammation and suggest a new model of TLR heterodimerization triggered by coreceptor signaling events.

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Authors: Stewart, C. R., Stuart, L. M., Wilkinson, K., van Gils, J. M., Deng, J., Halle, A., Rayner, K. J., Boyer, L., Zhong, R., Frazier, W. A., Lacy-Hulbert, A., Khoury, J. E., Golenbock, D. T., & Moore, K. J.
Affiliations: Harvard University (US)
University of Massachusetts Chan Medical School (US)
Washington University in St. Louis (US)
Corresponding author: Moore, Kathryn J
ORCID: Stewart, Cameron R
Stuart, Lynda M
Wilkinson, Kim
Deng, Jiusheng
Halle, Annett
Rayner, Katey J
Boyer, Laurent
Golenbock, Douglas T
Moore, Kathryn J
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2009-12-27
Volume: 11
Issue: 2
Pages: 155-161
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.1836
PMC: PMC2809046
OpenAlex: W2045772297
Cited by: 1,513
References: 42
Citations by year: 2026: 53 · 2025: 69 · 2024: 107 · 2023: 74 · 2022: 108 · 2021: 96 · 2020: 102 · 2019: 97 · 2018: 99 · 2017: 94 · 2016: 98 · 2015: 108 · 2014: 81 · 2013: 92 · 2012: 104
FWCI: 33.44
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
Data Archiving and Networked Services (DANS) (submittedVersion)
Leiden Repository (Leiden University) (submittedVersion)
MPG.PuRe (Max Planck Society) (submittedVersion)
Funders: Wellcome Trust (068089)
National Institute on Aging (R01AG20255, R01AG020255, R01AG032349)
National Institute of Allergy and Infectious Diseases (R01AI079198)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK043351)
National Institute of Neurological Disorders and Stroke (R01NS059005)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords: CD36, TLR4, TLR6, sterile inflammation, oxidized LDL, amyloid-beta, atherosclerosis, Alzheimer's disease, innate immune activation
MeSH terms: Animals, Cell Line, Humans, Inflammation, Lipoproteins, LDL, Mice, Inbred C57BL, Blotting, Western, Signal Transduction, Gene Expression, Amyloid beta-Peptides, Microglia, Mice, Knockout, Chemokines, CD36 Antigens, Reverse Transcriptase Polymerase Chain Reaction, Immunoprecipitation, Atherosclerosis, Toll-Like Receptor 4, Toll-Like Receptor 6, Mice

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CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer

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