Grant: CIHR Fellowship

Type 1 diabetes (T1D) is an autoimmune disease that occurs when the immune system attacks and destroys the beta cells in the pancreas. Beta cells are responsible for producing the hormone insulin, which regulates the levels of sugar in the blood. There is currently no cure for T1D. The immune system is responsible for protection of our bodies against infections and cancers. Immune cells are very sensitive to changes in the levels of sugar and other nutrients in the body, which changes in T1D. In this proposal, we will study how immune cells and cells in the pancreas communicate. This will enable us to understand why the immune system ends up killing our own insulin-producing cells, leading to T1D. We propose that changes in the nutritional environment surrounding beta cells may increase the response by immune cells, inducing an exaggerated immune attack and loss of beta cells. So, we will study nutrients and other factors that are secreted by beta cells and how these factors are received and metabolized by immune cells. We will study factors released by healthy beta cells, beta cells in diabetes, as well as beta cells that have been through stress such as high and low levels of sugar, or inflammatory stress. We will analyze how immune cells become activated after being exposed to these factors and try to turn off the pathways that are 'switched on' in immune cells in contact with stressed beta cells. Our project aims to identify new ways to control and slow down the progression of T1D by focusing on the interaction between immune cells and insulin-producing beta cells in the pancreas. We hope to gain a better understanding of how changes in metabolism in immune cells may lead to the immune attack on beta cells in T1D, and design ways to alter these metabolic pathways in immune cells to prevent or slow T1D.