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Updated: Jul 16, 2026
09:46
Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
Published on: December 27, 2017
Platelets recruit human dendritic cells via Mac-1/JAM-C interaction and modulate dendritic cell function in vitro
Harald F Langer1, Karin Daub, Gregor Braun
1Innere Medizin, Abteilung III, Eberhard Karls Universität Tübingen, Otfried-Müller Str. 10, 72076 Tübingen, Germany. harald.langer@med.uni-tuebingen.de
Arteriosclerosis, Thrombosis, and Vascular Biology
|March 24, 2007
Summary
Platelets recruit dendritic cells (DCs) to injured blood vessels, promoting DC maturation and platelet consumption. This interaction, involving specific adhesion molecules, may drive atherosclerosis progression.
Area of Science:
- Immunology
- Vascular Biology
- Atherosclerosis Research
Background:
- Thrombotic events and immunoinflammatory processes are intertwined in atherosclerotic lesion development.
- Understanding platelet-dendritic cell (DC) interactions is crucial for elucidating vascular remodeling mechanisms.
Purpose of the Study:
- To investigate the intricate interactions between platelets and dendritic cells (DCs).
- To determine the molecular mechanisms governing DC adhesion to platelets and their functional consequences.
Main Methods:
- Investigated DC rolling and adhesion to platelets using P-selectin glycoprotein ligand-1 (PSGL-1) and integrin alphaMbeta2 (Mac-1).
- Assessed in vivo DC recruitment to injured carotid arteries in mice.
- Evaluated DC maturation, lymphocyte proliferation, and phagocytosis upon coincubation with platelets.
- Examined the role of soluble GPVI and soluble JAM-C in DC-platelet interactions and DC apoptosis.
Main Results:
- DC rolling on platelets was PSGL-1 dependent, while firm adhesion involved integrin alphaMbeta2 (Mac-1).
- Platelets mediated DC adhesion to injured carotid arteries in vivo, reducible by soluble GPVI.
- Platelet-JAM-C interaction significantly reduced DC adhesion to platelets.
- Coincubation with platelets induced DC maturation (CD83 expression) and enhanced DC-driven lymphocyte proliferation.
- DCs phagocytosed platelets, and platelet/DC interaction led to DC apoptosis via a JAM-C-dependent pathway.
Conclusions:
- Platelet-mediated recruitment of DCs, via CD11b/CD18 (Mac-1) and platelet JAM-C, results in DC activation and platelet phagocytosis.
- This platelet-DC crosstalk is a significant factor in the progression of atherosclerotic lesions.
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Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
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As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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