Abstract
There is increasing evidence that oxidized phospholipids (OxPLs) play an important role in atherosclerosis. These phospholipids accumulate in human and mouse lesions. Specific OxPLs have been identified as major regulators of many cell types present in the vessel wall. In endothelial cells, >1,000 genes are regulated. Some of these genes are pro-atherogenic and others anti-atherogenic. The anti-atherogenic effects are likely important in slowing the atherogenic process. Several receptors and signaling pathways associated with OxPL action have been identified and shown to be upregulated in human lesions. A structural model of the mechanism by which specific OxPLs serve as CD36 ligands has been identified. Specific oxidized phospholipids are also present in plasma and associated with Lp(a) particles. In humans, OxPL/apolipoprotein B has been shown to be a prognostic indicator and a separate risk factor for coronary events. Levels of OxPL in plasma have been shown to be correlated with platelet activation. The results of these studies suggest an important role for OxPL in all stages of atherosclerosis.
Highlights
There is increasing evidence that oxidized phospholipids (OxPLs) play an important role in atherosclerosis
PEIPC accumulated in macrophages infected with live mycobacteria and inhibited expression of CD1b on differentiating dendritic cell (DC) leading to decreased antigen presentation
In addition to effects on DCs, OxPLs were shown to directly affect and induce anergy in T-cells [34]. These results show that a dyslipidemic microenvironment can directly interfere with DC and T-cell responses to pathogen-derived signals and skew the development of T-cell-mediated immunity
Summary
Departments of Pathology and Medicine,* University of California, Los Angeles, CA; Department of Pharmacology and the Robert Berne Center for Cardiovascular Research,† University of Virginia, Charlottesville, VA; and Department of Medicine,§ University of California, San Diego, CA
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