Abstract
Beyond their indispensable role in hemostasis, platelets have shown to affect the development of inflammatory disorders, as they have been epidemiologically and mechanistically linked to diseases featuring an inflammatory reaction in inflammatory diseases like multiple sclerosis, rheumatoid arthritis and inflammatory bowel disorders. The identification of novel molecular mechanisms linking inflammation and to platelets has highlighted them as new targets for therapeutic interventions. In particular, genetic and pharmacological studies have identified an important role for platelets in neuroinflammation. This review summarizes the main molecular links between platelets and inflammation, focusing on immune regulatory factors, receptors, cellular targets and signaling pathways by which they can amplify inflammatory reactions and that make them potential therapeutic targets.
Highlights
Platelets are tiny anucleate cells that circulate in a quiescent discoid state in the blood stream [1]
platelet MP (PMP), like platelets, expose a range of surface proteins which enable them both to provide binding sites for adjacent target cells and to deliver surrounded stimuli leading to the secretion of cytokines/chemokines, under the control of specific intracellular regulatory pathways
The relevance of P2Y12 receptor inhibitors like clopidogrel or prasugrel in Multiple sclerosis (MS) patients has not yet been analyzed, but platelets can bind to central nervous system (CNS)-specific lipid rafts through CD62P [31] and CD40 Ligand (CD40L) triggers endothelial activation [45], meaning both mediators fire neuroinflammatory processes
Summary
Platelets are tiny anucleate cells that circulate in a quiescent discoid state in the blood stream [1] Their well-known physiological function is to regulate hemostasis as cellular effectors of hemostasis. Dysregulation of the coagulation cascade can lead to an aberrant activation and, aggregation of platelets that is mostly associated with cardiovascular pathogenesis (reviewed in detail elsewhere [6,7,8,9]) In addition to their well-understood and indispensable hemostatic role, platelets are receiving more and more interest as immune and inflammatory effector cells [10]. PMP, like platelets, expose a range of surface proteins which enable them both to provide binding sites for adjacent target cells (e.g., leukocytes, endothelial cells) and to deliver surrounded stimuli leading to the secretion of cytokines/chemokines, under the control of specific intracellular regulatory pathways. Increased amounts of platelet-derived factors along with increased activation status of platelets occur in the pathogenesis of several immune mediated inflammatory diseases
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