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Updated: Jun 22, 2026
05:51
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Dendritic cells in atherosclerotic disease
Alexander Niessner1, Cornelia M Weyand
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. alexander.niessner@meduniwien.ac.at
Clinical Immunology (Orlando, Fla.)
|June 13, 2009
Summary
Dendritic cells (DC) are key immune players in atherosclerosis, driving plaque rupture. Activated myeloid and plasmacytoid DC promote inflammation and cell death, contributing to myocardial infarction.
Area of Science:
- Immunology
- Cardiovascular Biology
- Pathophysiology
Background:
- Atherosclerosis is increasingly recognized as an immune-mediated disease, moving beyond lipid storage theories.
- Dendritic cells (DC) bridge innate and adaptive immunity within atherosclerotic plaques.
Purpose of the Study:
- To elucidate the role of dendritic cells (DC) in atherogenesis.
- To highlight the specific contribution of DC to plaque rupture and myocardial infarction.
Main Methods:
- Review of current literature on DC subsets in atherosclerosis.
- Analysis of DC activation pathways and their downstream effects on plaque stability.
Main Results:
- Two DC subsets, myeloid DC (mDC) and plasmacytoid DC (pDC), are identified in atherosclerotic lesions.
- Activated DC, particularly pDC, produce type I interferon (IFN), upregulating TRAIL and inducing apoptosis of plaque-resident cells.
Conclusions:
- Dendritic cells play a critical role in the immune response within atherosclerotic plaques.
- DC-mediated inflammation and apoptosis contribute significantly to plaque rupture, a major cause of myocardial infarction.
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