Platelet Toll-Like Receptor Expression: The Link Between “Danger” Ligands and Inflammation

E-ISSN： 2212-4055|9|5|322-333

ISSN： 1871-5281

Source： Inflammation & Allergy-Drug Targets (Formerly Current Drug Targets - Inflammation & Allergy), Vol.9, Iss.5, 2010-12, pp. : 322-333

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Abstract

Platelets are non-nucleated cellular elements that play a role in hemostasis, innate immunity, and inflammation. Platelet-linked inflammation seems essentially related to the capacity of platelets to secrete cytokines, chemokines, and related molecules upon stimulation or state change. Moreover, platelets display receptors for numerous types of cytokines/chemokines, as well as immunoglobulins (FcγRI, II, III; FcεRI, II; FcRI/CD89). This secretory function confers to platelets a regulatory role in immunity. Platelets also exhibit non-self infectious danger detection molecules on their surfaces, particularly from the Toll-like receptor (TLR) family; through TLR expression, platelets can bind infectious agents and also deliver different signals for the secretion of cytokines and chemokines. Platelets may therefore be regarded as a neglected component of immune cell regulators, and they contribute to some interesting aspects in bridging innate and adaptive immunity. Recent investigations of the platelet TLR signalosome have been developed, and some studies have already confirmed the existence of a functional TLR/Myd88 pathway in platelets also (similar to as in eukaryotic nucleated cells). In eukaryotic cells, TLR adaptor and signalling proteins downstream of TLR activation typically represent a potential target on the Toll/Interleukin-1 receptor domain pathway for therapeutic drugs. Further, platelets may sense several types of infectious pathogens and limit microbial colonization by sequestering these pathogens and releasing immunomodulatory factors. This review aims to revisit some functions that platelets exert directly in antiinfection immunity; it presents experimentally-driven arguments in favor of a role for the TLR in regulating certain immune activities.