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Project Description
Type 1 Diabetes (T1D) is an autoimmune disease where the body’s own immune system attacks and destroys the insulin-producing beta cells in the pancreas. This leads to a cascade of disruptions in the body, making it difficult to regulate blood sugar levels.
The goal of this research project is to better understand the early stages of T1D development by exploring the role of extracellular vesicles (EVs) – small membrane-bound particles released by cells, including the pancreatic beta cells. These EVs carry important molecules that can provide insights into the health and status of the beta cells, and they make their way into the bloodstream where they can be detected and analyzed.
Specifically, we are interested in how the beta cells respond to inflammation, which is a key factor in the development of T1D. When under stress, the beta cells increase the production of a protein called programmed cell death-Ligand 1 (PD-L1), which helps regulate and mitigate the destruction of beta cells by the immune system. We want to understand how the beta cells package and release PD-L1 protein into EVs, and how this process may change as T1D progresses.
By analyzing the content and characteristics of these EVs released into the extracellular space and bloodstream, we hope to uncover valuable information about the state of the beta cells, potentially identifying early markers or mechanisms associated with the development of T1D. By delving deeper into the role of EV PD-L1 in the immune response in T1D, this study aims to establish EVs as potential blood-based biomarkers for the disease. Ultimately, this research could lead to the development of new interventions aimed at preventing the autoimmune destruction of beta cells in T1D. 
