John Libbey Eurotext



Neutrophil extracellular traps, hemostatsis and thrombosis Volume 23, issue 2, Mars-Avril 2017


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1 UMR CNRS 7292,
université François Rabelais,
Tours, France
2 Laboratoire d’hématologie-hémostase,
37044 Tours Cedex, France
3 Laboratoire d’hématologie,
CHU Reims, France
* Tirés à part

Polymorphonuclear cells (PMNC) are key cells of immunity. The production of Neutrophil Extracellular Traps (NETs) is consecutive to PMNC activation, which leads to the release of long DNA fragments decorated with highly diversified proteins. NETs have initially been described in infection control processes since they can trap and kill extra-cellular pathogens. NETs can also contribute to immunothrombosis, a pathogenic process involving the innate immune system and leading to thrombus formation. Actually, NETs were shown to be implicated in all main processes of hemostasis. They enhance platelet activation and aggregation, and promote the coagulation cascade by activating the contact pathway. NETs also inhibit physiologic inhibitors, and form a three-dimensional scaffold that helps fibrin clot formation. NETs also seem to confer fibrin clot resistance to fibrinolysis. Animal models suggested an implication of NETs in venous thrombosis, and in arterial thrombotic diseases such as atherosclerosis or ischemic stroke. Even if evidence for a critical role of NETS is more limited in human pathology, new targeted therapies could represent an alternative approach in specific diseases.