Department of Microbiology, Immunology and Infectious Diseases
Professor, Department of Microbiology, Immunology & Infectious DiseasesMicrobiology, Immunology & Infectious Diseases (MIID) Alberta Heritage Foundation for Medical Research Scientist Member, Diabetes & Endocrine Research Group Associate Member, Immunology Research Group Chair, Julia McFarlane Diabetes Research Centre Address: Health Research Innovation Centre Phone: (403) 220-8735 Fax: (403) 210-8862 Email: firstname.lastname@example.org
Potential Graduate Supervisor
Insulin-dependent diabetes mellitus (IDDM) results from a complex CD4+ and CD8+ T-cell-dependent autoimmune process directed against the insulin-producing beta cells of the pancreas. The mechanisms of beta cell destruction in IDDM and the mechanisms underlying the genetic predisposition and resistance to this autoimmune disease are issues of fundamental importance that remain unsolved. Research in my laboratory focuses on attempting to elucidate how, when and where diabetogenic T-cells differentiate into effector cells in vivo , to define the precise mechanisms through which they kill beta cells in the course of spontaneous disease, and to define the mechanisms of action of protective genes. With these objectives in mind, my laboratory has engineered nonobese diabetic mice (which develop a form of diabetes similar to human IDDM) to have immune systems in which virtual all T-cells are beta cell killers [transgenic nonobese diabetic (NOD) mice expressing the T-cell receptor (TCR) alpha and/or beta gene rearrangements of beta cell-specific CD4+ and CD8+ T-cell clones isolated from the pancreatic islets of NOD mice (4.1-NOD and 8.3-NOD mice, respectively)]. Since most of the T-cells maturing in these mice are beta cell-reactive, we can use these mice to investigate the effects of genes of interest (naturally occurring variants and altered forms of naturally-occurring variants) on the biology and disease-causing potential of diabetogenic T-cells. In the end, our wish is to help define potential targets for therapeutic intervention in human autoimmune diabetes.