Platelets and the innate immune system: mechanisms of bacterial-induced platelet activation.
J Thromb Haemost
; 9(6): 1097-107, 2011 Jun.
Article
in En
| MEDLINE
| ID: mdl-21435167
ABSTRACT
It has become clear that platelets are not simply cell fragments that plug the leak in a damaged blood vessel; they are, in fact, also key components in the innate immune system, which is supported by the presence of Toll-like receptors (TLRs) on platelets. As the cells that respond first 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 antimicrobial peptides. The main platelet receptors that mediate these interactions are glycoprotein (GP)IIb-IIIa, GPIbα, FcγRIIa, complement receptors, and TLRs. This process 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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Blood Platelets
/
Platelet Activation
/
Immunity, Innate
Limits:
Humans
Language:
En
Journal:
J Thromb Haemost
Journal subject:
HEMATOLOGIA
Year:
2011
Document type:
Article
Affiliation country:
Ireland