Role of complement activation in Heparin-induced thrombocytopenia | Shiv Nadar University
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Role of complement activation in Heparin-induced thrombocytopenia

Event Date: 
Thursday, July 14, 2022 - 00:00

Heparin is a commonly used anticoagulant agent for patients presenting with thrombotic disease. Some patients who receive heparin develop an immune-mediated thrombotic disorder called Heparin Induced Thrombocytopenia (HIT). HIT is caused by antibodies to a multimeric antigenic complex consisting of a positively charged protein, platelet factor 4 (PF4) and heparin, a negatively charged polysaccharide. Once these anti PF4/heparin antibodies are formed in the patients, they make immune complexes with PF4/heparin complexes and induce cellular activation, which leads to thrombotic events in the patients. Thrombosis is the most serious and life-threatening complication of HIT. Therapeutic interventions which can either inhibit the anti PF4/heparin antibody formation or cellular activation by these antibodies can avoid the harmful effects of this drug in the patients. The mechanisms that incite antibody production against PF4/heparin complexes in these patients and the mechanism of cellular activation and thrombosis in these patients are not completely understood. For the last few years, our goal has been to understand (A) the mechanism of immune activation and anti PF4/heparin antibody generation by PF4/heparin complexes and (B) the mechanism of cellular activation and thrombosis in HIT.

Thursday 14, Jul 2022

 
D-330

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