Platelets as Immune Cells: Bridging Inflammation and Cardiovascular Disease
[Reviews]
von Hundelshausen, Philipp; Weber, Christian
From the Institute of Cardiovascular Molecular Research, University Hospital of the Rheinisch-Westfälische Technische Hochschule, Aachen, Germany.
Original received September 28, 2006; revision received November 2, 2006; accepted November 6, 2006.
Correspondence to Dr Christian Weber, Institut für Kardiovaskuläre Molekularbiologie, Pauwelsstrasse 30, 52074 Aachen, Germany. E-mail cweber@ukaachen.de
Abstract—
Beyond an eminent role in hemostasis and thrombosis, platelets are characterized by expert functions in assisting and modulating inflammatory reactions and immune responses. This is achieved by the regulated expression of adhesive and immune receptors on the platelet surface and by the release of a multitude of secretory products including inflammatory mediators and cytokines, which can mediate the interaction with leukocytes and enhance their recruitment. In addition, platelets are characterized by an enormous surface area and open canalicular system, which in concert with specialized recognition receptors may contribute to the engulfment of serum components, antigens, and pathogens. Platelet-dependent increases in leukocyte adhesion may not only account for an exacerbation of atherosclerosis, for arterial repair processes, but also for lymphocyte trafficking during adaptive immunity and host defense. This review compiles a selection of platelet-derived tools for bridging inflammation and vascular disease and highlights the molecular key components governing platelet-mediated mechanisms operative in immune surveillance, vascular remodeling, and atherosclerosis.
Figure 1. Platelet adhesion molecules and surface receptors. For clarity, the symbols for the various protein domains depicted are explained within the Figure.
Figure 2. Platelet-derived soluble immune mediators. In addition to stimulating signal transduction, shape change, adhesion, and aggregation of platelets, the activation of platelets can result in the release of multiple and diverse soluble mediators with pleiotropic functions in inflammation.
Figure 3. Interactions of platelets with different leukocyte subtypes regulate vascular inflammation. A multitude of molecular mechanisms and platelet-derived components mediate and regulate platelet-induced leukocyte infiltration including chemokine deposition and mononuclear and endothelial cell activation. Depicted are examples of the variety of mechanisms and key elements described in greater detail in the text.
[Reviews]
von Hundelshausen, Philipp; Weber, Christian
From the Institute of Cardiovascular Molecular Research, University Hospital of the Rheinisch-Westfälische Technische Hochschule, Aachen, Germany.
Original received September 28, 2006; revision received November 2, 2006; accepted November 6, 2006.
Correspondence to Dr Christian Weber, Institut für Kardiovaskuläre Molekularbiologie, Pauwelsstrasse 30, 52074 Aachen, Germany. E-mail cweber@ukaachen.de
Abstract—
Beyond an eminent role in hemostasis and thrombosis, platelets are characterized by expert functions in assisting and modulating inflammatory reactions and immune responses. This is achieved by the regulated expression of adhesive and immune receptors on the platelet surface and by the release of a multitude of secretory products including inflammatory mediators and cytokines, which can mediate the interaction with leukocytes and enhance their recruitment. In addition, platelets are characterized by an enormous surface area and open canalicular system, which in concert with specialized recognition receptors may contribute to the engulfment of serum components, antigens, and pathogens. Platelet-dependent increases in leukocyte adhesion may not only account for an exacerbation of atherosclerosis, for arterial repair processes, but also for lymphocyte trafficking during adaptive immunity and host defense. This review compiles a selection of platelet-derived tools for bridging inflammation and vascular disease and highlights the molecular key components governing platelet-mediated mechanisms operative in immune surveillance, vascular remodeling, and atherosclerosis.
Figure 1. Platelet adhesion molecules and surface receptors. For clarity, the symbols for the various protein domains depicted are explained within the Figure.
Figure 2. Platelet-derived soluble immune mediators. In addition to stimulating signal transduction, shape change, adhesion, and aggregation of platelets, the activation of platelets can result in the release of multiple and diverse soluble mediators with pleiotropic functions in inflammation.
Figure 3. Interactions of platelets with different leukocyte subtypes regulate vascular inflammation. A multitude of molecular mechanisms and platelet-derived components mediate and regulate platelet-induced leukocyte infiltration including chemokine deposition and mononuclear and endothelial cell activation. Depicted are examples of the variety of mechanisms and key elements described in greater detail in the text.
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