HIT-IgGs Induce a Heparin-Dependent Pro-Thrombotic Phenotype in a Novel Endothelialized Microfluidic Disease Model

Introduction Heparin-induced thrombocytopenia (HIT) is a serious adverse reaction to heparin. Heparin/PF4/IgG complexes have been reported to activate platelets, neutrophils, and possibly endothelial cells, resulting in thrombocytopenia, hypercoagulability and thromboembolic complications. While the impact of anti-PF4/heparin antibodies on blood cell activation has been extensively studied, the role of endothelial cells in HIT-associated thrombosis remains underexplored. In particular, the interactions between HIT-induced procoagulancy and endothelial cells under flow conditions is not completely elucidated. In this report, we investigated how HIT antibodies induce thrombosis in an endothelialized microfluidic system.