Journal
NATURE IMMUNOLOGY
Volume 11, Issue 2, Pages 155-U75Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1836
Keywords
-
Categories
Funding
- US National Institutes of Health [R01AG20255, R01NS059005, R01 AG032349]
- Ellison Medical Foundation
- American Health Assistance Foundation [A2008-130]
- Wellcome Trust [068089/Z/02/Z]
Ask authors/readers for more resources
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.
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