Grant: Operating Grant

Type 1 diabetes (T1D) is an autoimmune disease in which an individual's own immune system selectively targets and destroys pancreatic islet cells. The loss of pancreatic islet cells, required for insulin production and the control of blood sugar levels, results in insulin insufficiency, hyperglycemia and eventually, serious complications that accompany the inability to regulate blood sugar levels. While details of the T1D disease process remain poorly understood, it is known that both genetic and environmental factors play critical roles in the development of this disorder. Recently, several independent research teams have identified a genetic variant of a novel gene called CLEC16A that is tightly associated with T1D. Furthermore, gene variants of CLEC16A have been recently associated with other autoimmune diseases, like multiple sclerosis, primary adrenal insufficiency and autoimmune thyroid disease. These findings along with CLEC16A's exclusive gene expression in immune cells suggest that it is likely involved in the pathogenesis of autoimmune disease through its effects on immune cell function. However, there is virtually nothing known about CLEC16A or how it may impact immunity and autoimmunity. Our research proposal is focused on the investigation of CLEC16A function and describes a number of key strategies to elucidate the physiological role of this gene. Knowledge of CLEC16A function will lead to important insight into the pathogenesis of T1D and may lead to new avenues of T1D prevention through modulation of its function.