2016/06/29 by Laura L. Swystun, Patricia C. Liaw · 3 citations
Medicine · Immunology and Microbiology · #Platelet Disorders and Treatments #Neutrophil, Myeloperoxidase and Oxidative Mechanisms #Venous Thromboembolism Diagnosis and Management #Thrombogenicity #Coagulation #Thrombus #Platelet #Platelet activation #Fibrinolysis #Tissue factor #Proinflammatory cytokine #Immunology #Cell biology #Inflammation #Immune system #Cell adhesion molecule #Medicine #Biology #Internal medicine
paper · pdf · doi:10.1182/blood-2016-05-718114
openalex publication_date 2016/06/29 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/15
In recent years, the traditional view of the hemostatic system as being regulated by a coagulation factor cascade coupled with platelet activation has been increasingly challenged by new evidence that activation of the immune system strongly influences blood coagulation and pathological thrombus formation. Leukocytes can be induced to express tissue factor and release proinflammatory and procoagulant molecules such as granular enzymes, cytokines, and damage-associated molecular patterns. These mediators can influence all aspects of thrombus formation, including platelet activation and adhesion, and activation of the intrinsic and extrinsic coagulation pathways. Leukocyte-released procoagulant mediators increase systemic thrombogenicity, and leukocytes are actively recruited to the site of thrombus formation through interactions with platelets and endothelial cell adhesion molecules. Additionally, phagocytic leukocytes are involved in fibrinolysis and thrombus resolution, and can regulate clearance of platelets and coagulation factors. Dysregulated activation of leukocyte innate immune functions thus plays a role in pathological thrombus formation. Modulation of the interactions between leukocytes or leukocyte-derived procoagulant materials and the traditional hemostatic system is an attractive target for the development of novel antithrombotic strategies.