Jaileene Hernandez Escalante
B.S. in Biology, Temple University
T1D is an autoimmune disorder involving the destruction of pancreatic β cells by autoreactive T cells leading to a loss of insulin production and control of blood glucose levels. While genetic components to the disease exist, there is evidence that environmental factors may play a role in disease progression. Abnormalities in lipid metabolism often occur in T1D patients and I am interested in how metabolic environmental effects contribute to Type 1 Diabetes (T1D) disease progression. My dissertation research in Dr. Hans Dooms’ lab will be to understand the effect of different chain length fatty acids on phenotype and function of T cells from the non-obese diabetic (NOD) mouse model along with the effects on disease pathogenesis. The T cell metabolic program promptly changes depending on the activation state of cells and influences T cell phenotype. These metabolic programs match T cell function where T helper Th1 and Th2 cells rely on glycolysis to carry out their roles while CD8+ memory and T regulatory cells depend on fatty acid oxidation and oxidative phosphorylation. We are working to understand how changes in the cell-extrinsic metabolic environment as well as cell-intrinsic defects in metabolic pathways may alter T cell responses and promote autoimmunity.