The process of β-cell decline in the lead-up to the overt diabetes could provide critical clues for timely therapeutic intervention. However the complexity, cell-type specificity, rapidly changing dynamics and the cumulative effects of inflammation all inform the outcome of the autoimmune attack on beta cell.

This proposal is designed to use multiple in vitro models systems of beta cell inflammation, along with human tissue samples as well as human serum samples from T1D children, to arrive at a temporal proteomic and metabolomics profile of human islet inflammation and death. These data are likely to contribute towards our understanding of biomarkers that would assist in staging the progression of human type 1 diabetes. The ultimately goal is to be able to use the information gleaned from the grant to identify windows of opportunity when therapeutic intervention could preserve beta cell mass and function to delay the progression towards full-blown diabetes.