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Description:
This session will highlight recent developments in this field that have uncovered key features of the underlying immunological mechanisms responsible for DHTRs, TRALI, and HIT with implications in more effective treatment and prevention strategies.
Dr. Satheesh Chonat will discuss the role of complement in the development of DHTRs with hyperhemolysis and the underlying pathophysiology of SCD in general. By leveraging a series of translational studies and preclinical models, he will discuss the underlying the susceptibility of Sickle RBCs and endothelium to complement-mediated injury during transfusion-associated hemolysis and other SCD complications, while also exploring the potential role of complement inhibitory approaches in the treatment of acute SCD complications.
Dr. Rick Kapur will define key features of the underlying pathophysiology of TRALI, with a particular focus on the role of complement in this transfusion reaction. Data generated from clinical and preclinical studies will be presented that focus on the role of complement in facilitating macrophage activation and neutrophil-extracellular trap formation that ultimately contributes to the development of TRALI.
Dr. Demin Wang will focus on the pathophysiology of HIT. He will provide an overview of the immune pathogenesis of HIT and the origin of B cells that produce protein platelet factor 4 (PF4) in a complex with heparin (H)-specific antibodies. He will also explore how the breakdown of B cell peripheral tolerance contributes to the production of pathogenic PF4/H-specific antibodies. He will then highlight the molecular and functional properties of pathogenic PF4/H-specific antibodies and offer new approaches to the diagnosis and treatment of this condition.
Dr. Satheesh Chonat will discuss the role of complement in the development of DHTRs with hyperhemolysis and the underlying pathophysiology of SCD in general. By leveraging a series of translational studies and preclinical models, he will discuss the underlying the susceptibility of Sickle RBCs and endothelium to complement-mediated injury during transfusion-associated hemolysis and other SCD complications, while also exploring the potential role of complement inhibitory approaches in the treatment of acute SCD complications.
Dr. Rick Kapur will define key features of the underlying pathophysiology of TRALI, with a particular focus on the role of complement in this transfusion reaction. Data generated from clinical and preclinical studies will be presented that focus on the role of complement in facilitating macrophage activation and neutrophil-extracellular trap formation that ultimately contributes to the development of TRALI.
Dr. Demin Wang will focus on the pathophysiology of HIT. He will provide an overview of the immune pathogenesis of HIT and the origin of B cells that produce protein platelet factor 4 (PF4) in a complex with heparin (H)-specific antibodies. He will also explore how the breakdown of B cell peripheral tolerance contributes to the production of pathogenic PF4/H-specific antibodies. He will then highlight the molecular and functional properties of pathogenic PF4/H-specific antibodies and offer new approaches to the diagnosis and treatment of this condition.