Platelets as immune cells - Bridging inflammation and cardiovascular disease

被引:565
作者
von Hundelshausen, Philipp [1 ]
Weber, Christian [1 ]
机构
[1] Univ Hosp, Rhein Westfal TH Aachen, Inst Cardiovasc Mol Res, D-5100 Aachen, Germany
关键词
platelets; inflammation; cardiovascular disease; chemokines; adhesion molecules;
D O I
10.1161/01.RES.0000252802.25497.b7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:27 / 40
页数:14
相关论文
共 203 条
[51]   Prominent role of P-selectin in the development of advanced atherosclerosis in apoE-deficient mice [J].
Dong, ZM ;
Brown, AA ;
Wagner, DD .
CIRCULATION, 2000, 101 (19) :2290-2295
[52]  
DRIPPS DJ, 1991, J BIOL CHEM, V266, P10331
[53]   Platelet factor 4 promotes adhesion of hematopoietic progenitor cells and binds EL-8: novel mechanisms for modulation of hematopoiesis [J].
Dudek, AZ ;
Nesmelova, I ;
Mayo, K ;
Verfaillie, CM ;
Pitchford, S ;
Slungaard, A .
BLOOD, 2003, 101 (12) :4687-4694
[54]   EXPERIMENTAL BACTERIAL-ENDOCARDITIS .4. STRUCTURE AND EVOLUTION OF VERY EARLY LESIONS [J].
DURACK, DT .
JOURNAL OF PATHOLOGY, 1975, 115 (02) :81-+
[55]   Cooperation between platelet-derived CD154 and CD4+ T cells for enhanced germinal center formation [J].
Elzey, BD ;
Grant, JF ;
Sinn, HW ;
Nieswandt, B ;
Waldschmidt, TJ ;
Ratliff, TL .
JOURNAL OF LEUKOCYTE BIOLOGY, 2005, 78 (01) :80-84
[56]   Platelet-mediated modulation of adaptive immunity: A communication link between innate and adaptive immune compartments [J].
Elzey, BD ;
Tian, J ;
Jensen, RJ ;
Swanson, KA ;
Lees, JR ;
Lentz, SR ;
Stein, CS ;
Nieswandt, B ;
Wang, YQ ;
Davidson, BL ;
Ratliff, TL .
IMMUNITY, 2003, 19 (01) :9-19
[57]  
ERICKSON PR, 1993, J BIOL CHEM, V268, P1646
[58]  
ERICKSON PR, 1992, J BIOL CHEM, V267, P10018
[59]   The interaction of bacterial pathogens with platelets [J].
Fitzgerald, J. Ross ;
Foster, Timothy J. ;
Cox, Dermot .
NATURE REVIEWS MICROBIOLOGY, 2006, 4 (06) :445-457
[60]   Fibronectin-binding proteins of Staphylococcus aureus mediate activation of human platelets via fibrinogen and fibronectin bridges to integrin GPIIb/IIIa and IgG binding to the FcγRIIa receptor [J].
Fitzgerald, JR ;
Loughman, A ;
Keane, F ;
Brennan, M ;
Knobel, M ;
Higgins, J ;
Visai, L ;
Speziale, P ;
Cox, D ;
Foster, TJ .
MOLECULAR MICROBIOLOGY, 2006, 59 (01) :212-230