T1D is defined classically as autoimmune-mediated destruction of the insulin producing β cells. However, recent data from the lab and other researchers around the world indicate an important role for pathways intrinsic to the β cell that may accelerate the development of diabetes. These data suggest that processes in the β cell, such as calcium dyshomeostasis, altered protein folding, oxidative and ER stress, and changes in the miRNA and gene expression patterns occur early during the initiation and evolution of T1D. These pathways then act to augment autoimmune-mediated β cell death by increasing β cell immunogenicity.
In addition to ongoing work aimed at identifying and intervening on these molecular pathways, the lab is also working to define signatures of β cell stress to identify those at risk of developing T1D. Work in this area is part of the Human Islet Research Network