Plasmacytoid Dendritic Cells in Atherosclerosis: Knocking at T-Cell's Door
The contribution of both innate and adaptive immune processes to the pathophysiology of atherosclerosis is undisputed. Next to cytokines, a range of danger-associated molecular pattern molecules (DAMP) are being released in plaque, amongst others by apoptotic and necrotic cells and due to proteolysis of extracellular matrix material. These proinflammatory agents will activate several leukocyte populations to perpetuate the inflammatory process1. Even healthy vessels harbor subendothelial networks of several dendritic cell (DCs) subsets, which are considerably expanded in atherosclerosis2. DCs orchestrate innate and adaptive immunity against invading pathogens as well as altered self-antigens and have been attributed a central role in atherosclerosis-related immune responses. Nevertheless, considerable controversy exists about the phenotype of discrete DC subsets in and their impact on atherosclerosis. Genetic manipulation studies in which the total pool of conventional DCs (cDCs) was ablated or expanded gave rather inconsistent results. These studies not only left unaddressed if particular cDC subsets play a dominant role in the control of adaptive immune responses relevant to atherosclerosis or of cholesterol homeostasis3, 4, they also urged for more refined approaches targeting specific subsets of this heterogeneous cell population.
- Received September 7, 2014.
- Accepted September 8, 2014.