Abstract

Atherosclerosis has been considered a syndrome of dysregulated lipid storage until recent evidence has emphasized the critical contribution of the immune system. Dendritic cells (DC) are positioned at the interface of the innate and adaptive immune system. Recognition of danger signals in atheromas leads to DC activation. Activated DC regulate effector T cells which can kill plaque-resident cells and damage the plaque structure. Two types of DC have been identified in atherosclerotic lesions; classical myeloid DC (mDC) which mainly recognize bacterial signatures and plasmacytoid DC (pDC) which specialize in sensing viral fragments and have the unique potential of producing large amounts of type I interferon (IFN). In human atheromas, type I IFN upregulates expression of the cytotoxic molecule TRAIL which leads to apoptosis of plaque-resident cells. This review will elucidate the role of DC in atherogenesis and particularly in plaque rupture, the underlying pathophysiologic cause of myocardial infarction.

View details for DOI 10.1016/j.clim.2009.05.006

View details for Web of Science ID 000273696600003

View details for PubMedID 19520615