Mentor: Dr. Clayton Mathews
College of Medicine
"Research has helped enrich what I learn in classroom settings while helping me establish scientific foundations in hypothesis development and testing."
- Immunopathogenesis of T1D
Hobbies and Interests
Type I Interferon on Beta Cell Death
Previous studies by my mentor using a mouse model that develops a human-like spontaneous Type 1 diabetes, Non-obese diabetic (NOD) mice, has shown that INFα/β producing plasmacytoid dendritic cells are found adjacent to β cells that have lost expression for an essential transporter for glucose-stimulated insulin secretion, GLUT2. Further, in vitro studies have confirmed that that IFNα significantly down regulates Glut2 mRNA in the NOD derived β cell line, NIT-1. Additionally, treatment of isolated islets from NOD-Rag1-/- mice with IFNα or IFNβ resulted in a significant decline in glucose stimulated insulin secretion (GSIS), compared to IFNγ or untreated islets. These studies in NOD mice strongly support the postulate that IFNα/β is also responsible for the decrease GSIS prior to the onset of TID in humans. We therefore hypothesize that after IFNα/β bind to the Interferon α/β Receptor (IFNAR) on β cells, the signaling pathways lead to a decreased expression of proteins that are essential for GSIS and an enhanced potential for immune surveillance. In short, we anticipate that IFNα/β drive dysfunction and immune-mediated death of β cells during the pathogenesis of T1D. By immunofluorescent staining, I aim to compare expression of IFNα/β signature proteins (MDA5, BST2, OAS1/2 or MXA/MXB) as well as proteins associated with insulin secretion (insulin, glucokinase, mitochondrial ATP synthase, and glucose transporters) in order to establish the correlation of Type I IFN signaling proteins with changes in proteins essential for insulin secretion.