Abstract
Platelets are anucleate cytoplasmic fragments derived from the fragmentation of medullary megakaryocytes. Activated platelets adhere to the damaged endothelium by means of glycoproteins on their surface, forming the platelet plug. Activated platelets can also secrete the contents of their granules, notably the growth factors contained in the α-granules, which are involved in platelet aggregation and maintain endothelial activation, but also contribute to vascular repair and angiogenesis. Platelets also have a major inflammatory and immune function in antibacterial defence, essentially through their Toll-like Receptors (TLRs) and Sialic acid-binding immunoglobulin-type lectin (SIGLEC). Platelet activation also contributes to the extensive release of anti- or pro-inflammatory mediators such as IL-1β, RANTES (Regulated on Activation, Normal T Expressed and Secreted) or CD154, also known as the CD40-ligand. Platelets are involved in the direct activation of immune cells, polynuclear neutrophils (PNNs) and dendritic cells via the CD40L/CD40 complex. As a general rule, all of the studies presented in this review show that platelets are capable of covering most of the stages of inflammation, primarily through the CD40L/CD40 interaction, thus confirming their own role in this pathophysiological condition.
Highlights
Blood platelets are anucleate cells produced by the fragmentation of megakaryocytes (MK)
Given i) the large blood platelet count, taking all vascular cellular elements into consideration, ii) their wide range of immune receptors, iii) the ability of platelets to interact with/promote immune cells and endothelial cells, and iv) their active participation in immunity and inflammation, blood platelets have been the subject of numerous investigations into the physiological processes related to inflammation
All of the studies presented in this review show that platelets are capable of covering most of the stages of inflammation, primarily through the CD40 ligand (CD40L)/CD40 interaction, confirming their own role in this pathophysiological condition
Summary
Blood platelets are anucleate cells produced by the fragmentation of megakaryocytes (MK). IL-1b activates endothelial cells causing increases in chemokine secretion and in the expression of molecules that trigger neutrophil and monocyte adhesion to the endothelium [25]. They demonstrated that platelets activated by an agonist express CD40L which triggers an inflammatory response in CD40 expressing endothelial cells.
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