Project 175805

Type 1 Diabetes (T1D) is a serious disorder of blood sugar regulation resulting from destruction of insulin-producing cells in the pancreas. In T1D, one's own immune system attacks the insulin-producing cells and destroys them, rendering the individual unable to produce insulin. Scientists do not know exactly what causes the immune system to attack the body's own cells in this way, but it is clear that both genetic and environmental factors are involved. There is little we can do to affect the heritable aspects of T1D susceptibility, but identifying environmental factors that trigger the autoimmune responses in genetically vulnerable individuals may be of help in preventing the disease. In this application, we propose an experiment to investigate whether air pollution could be a factor in promoting the autoimmune responses of T1D. Air pollution has been shown in other studies to promote the development of allergic responses, and in autoimmune diseases like rheumatoid arthritis. It is reasonable to hypothesize that it may have the same effect on the development of T1D. Mice that are genetically prone to develop T1D will be exposed to air pollution in the form of diesel engine exhaust particles, and the speed at which they develop diabetes and the severity of their autoimmune responses will be compared to diabetes-prone mice unexposed to pollution. We hypothesize that diabetes-prone mice exposed to air pollution will develop diabetes faster and have stronger autoimmune responses than mice not exposed. Given that the current treatments for T1D result in a notably reduced quality of life, we wish to identify factors promoting T1D so that we can reduce exposure to those factors. If air pollution can trigger T1D, it would provide evidence to support efforts to devise more appropriate air pollution emission guidelines in order to protect human health.