Innate Immunity

Biography

Biography: Cécile Oury

Abstract

This lecture will present the latest findings on the contribution of innate immune cells in thrombosis. It will also address the recent view of platelets as rapid first-line immune responders. Focus will be made on the role of P2X1 receptors for extracellular ATP. It has long been recognized that inflammation shifts the hemostatic mechanisms in favor of thrombosis. Upon tissue damage or infection, a sudden increase of extracellular ATP occurs, that might contribute to the crosstalk between inflammation and thrombosis. On platelets, P2X1 receptors act to amplify platelet activation and aggregation induced by other platelet agonists. These receptors critically contribute to thrombus stability in small arteries. Besides platelets, studies by our group indicate that these receptors are expressed by neutrophils. They promote neutrophil chemotaxis, both in vitro and in vivo. In a laser-induced injury mouse model of thrombosis, it appears that neutrophils are required to initiate thrombus formation and coagulation activation on inflamed arteriolar endothelia. In this model, by using P2X1-/- mice, we recently showed that P2X1 receptors, expressed on platelets and neutrophils, play a key role in thrombus growth and fibrin generation. Taken together, these data suggest that P2X1 receptors are involved in the interplay between platelets and neutrophils. Activation of these receptors by ATP on neutrophils and platelets might be involved in the regulation of inflammation, immunity and thrombosis.