• Hematology and Immunology
• Immunocamouflage of Blood Cells – Red Blood Cells, Leukocytes, and Platelets
• Redox-Mediated Erythrocyte Injury
• Anti-Viral Prophylaxis
• Iron Chelators

Dr. Scott’s laboratory is primarily focused on three primary areas of research: 1) investigation of the potential therapeutic use of “immunocamouflaged” cells/tissues in transfusion and transplantation medicine; 2) prevention of viral invasion via viral inactivation and target cell modification via immunocamouflage; and 3) examining whether the intraerythrocytic chelation and redox-inactivation of the hemoglobin-derived heme and iron present in the sickle and thalassemic RBC can slow/prevent premature red cell destruction.

Immunocamouflage of foreign cells and tissues is accomplished via the covalent modification of the cell membrane with nonimmunogenic materials such as methoxypoly(ethylene glycol). This nonimmunogenic barrier prevents the recognition of antigenic sites on the cell membrane by preexisting antibodies –hence preventing immunological rejection – and significantly diminishes the immunogenicity of the foreign cellular epitopes. Ongoing projects within the laboratory include the modification of red blood cells to prevent alloimmunization in the chronically transfused (e.g., sickle cell, thalassemic, autoimmune hemolytic anemia) patient; the prevention of graft versus host disease via lymphocyte modification; and the modification of pancreatic islets for tissue transplantation in diabetes.

Immunocamouflage also has application in the inactivation of viruses and/or prevention of viral infections. Studies in Dr. Scott’s laboratory have demonstrated the utility of the immunocamouflage technique in inactivation viruses contained in blood products by preventing normal cellular invasion. Similarly, the immunocamouflage of the target cells of viruses has also proven effective in preventing viral invasion and infection. The utility of this technology towards blood borne and respiratory (e.g., Rhinoviruses) viruses are actively under investigation.

Additional research in Dr. Scott’s laboratory is directed towards determining whether the intraerythrocytic chelation and redox-inactivation of the hemoglobin-derived heme and iron present in the sickle and thalassemic RBC may significantly delay its premature destruction. Previous studies by this laboratory have demonstrated that the basic pathophysiology of the sickle and thalassemic RBC is mediated by a self-propagating, self-amplifying redox reaction initiated by the initial autoxidation of the sickle hemoglobin or unpaired alpha and beta hemoglobin chains. Subsequent glutathione-driven, iron-mediated, oxidative events degrade additional hemoglobin (releasing more heme/Fe) as well as other cellular components leading to significant functional and structural changes. It is hypothesized that a modest prolongation of the life span of the thalassemic erythrocyte may improve the “effective” erythropoiesis (i.e., hematocrit, reticulocyte count) such that the need for transfusion therapy may be obviated in a significant segment of the thalassemic population.