Platelets and the innate immune system: Mechanisms of bacterial-induced platelet activation

Research output: Contribution to journalArticle

Standard

Platelets and the innate immune system: Mechanisms of bacterial-induced platelet activation. / Cox, D; Kerrigan, S; Watson, Steve.

In: Journal of Thrombosis and Haemostasis, Vol. 9, No. 6, 01.01.2010, p. 1097-1107.

Research output: Contribution to journalArticle

Harvard

APA

Vancouver

Author

Bibtex

@article{1ad0554f0ee04b50ac09b50c4ca10c25,
title = "Platelets and the innate immune system: Mechanisms of bacterial-induced platelet activation",
abstract = "It has become clear that platelets are not simply cell fragments that can plug the leak in a damaged blood vessel, they are in fact key components in the innate immune system which is supported by the presence of Toll-like receptors (TLRs) on platelets. As the first responding cell to a site of injury they are well placed to direct the immune response to deal with any resulting exposure to pathogens. The response is triggered by bacteria binding to platelets which usually triggers platelet activation and the secretion of anti-microbial peptides. The main  platelet receptors that mediate these interactions are GPIIb/IIIa, GPIbα, FcνRIIa, complement receptors and TLRs. This may involve direct interactions between bacterial proteins and the receptors or can be mediated by plasma proteins such as fibrinogen, von Willebrand factor, complement and IgG. Here we review the variety of interactions between platelets and bacteria and look at the potential for inhibiting these interactions in diseases such as infective endocarditis and sepsis.",
author = "D Cox and S Kerrigan and Steve Watson",
year = "2010",
month = jan,
day = "1",
doi = "10.1111/j.1538-7836.2011.04264.x",
language = "English",
volume = "9",
pages = "1097--1107",
journal = "Journal of Thrombosis and Haemostasis",
issn = "1538-7933",
publisher = "Wiley",
number = "6",

}

RIS

TY - JOUR

T1 - Platelets and the innate immune system: Mechanisms of bacterial-induced platelet activation

AU - Cox, D

AU - Kerrigan, S

AU - Watson, Steve

PY - 2010/1/1

Y1 - 2010/1/1

N2 - It has become clear that platelets are not simply cell fragments that can plug the leak in a damaged blood vessel, they are in fact key components in the innate immune system which is supported by the presence of Toll-like receptors (TLRs) on platelets. As the first responding cell to a site of injury they are well placed to direct the immune response to deal with any resulting exposure to pathogens. The response is triggered by bacteria binding to platelets which usually triggers platelet activation and the secretion of anti-microbial peptides. The main  platelet receptors that mediate these interactions are GPIIb/IIIa, GPIbα, FcνRIIa, complement receptors and TLRs. This may involve direct interactions between bacterial proteins and the receptors or can be mediated by plasma proteins such as fibrinogen, von Willebrand factor, complement and IgG. Here we review the variety of interactions between platelets and bacteria and look at the potential for inhibiting these interactions in diseases such as infective endocarditis and sepsis.

AB - It has become clear that platelets are not simply cell fragments that can plug the leak in a damaged blood vessel, they are in fact key components in the innate immune system which is supported by the presence of Toll-like receptors (TLRs) on platelets. As the first responding cell to a site of injury they are well placed to direct the immune response to deal with any resulting exposure to pathogens. The response is triggered by bacteria binding to platelets which usually triggers platelet activation and the secretion of anti-microbial peptides. The main  platelet receptors that mediate these interactions are GPIIb/IIIa, GPIbα, FcνRIIa, complement receptors and TLRs. This may involve direct interactions between bacterial proteins and the receptors or can be mediated by plasma proteins such as fibrinogen, von Willebrand factor, complement and IgG. Here we review the variety of interactions between platelets and bacteria and look at the potential for inhibiting these interactions in diseases such as infective endocarditis and sepsis.

U2 - 10.1111/j.1538-7836.2011.04264.x

DO - 10.1111/j.1538-7836.2011.04264.x

M3 - Article

C2 - 21435167

VL - 9

SP - 1097

EP - 1107

JO - Journal of Thrombosis and Haemostasis

JF - Journal of Thrombosis and Haemostasis

SN - 1538-7933

IS - 6

ER -