Principal Investigator: Jonathan Katz, PhD
Type 1 diabetes, also known as childhood diabetes, autoimmune diabetes or juvenile diabetes, is the most common autoimmune disease in children. This disease is on the rise in the developed world, especially among individuals of European descent. Cincinnati Children’s had almost 9,000 inpatient and outpatient visits related to T1D just last year.
This disease has no cure and the only current therapy is insulin-replacement, normally by multi-daily insulin injections or the use of an insulin pump. Children with T1D have a number of psycho-social issues above and beyond the increased risk for secondary physical complications including blindness, amputation and cardiovascular problems. T1D is understood to be an autoimmune disease in which immune cells recognize and destroy the insulin producing beta cells resulting in high blood sugar. The disease has both a genetic and environmental component. While much is being learned about the genetics that underlie the disease, little is known about how these genetic changes lead to T1D. More importantly, less is known about the environmental component nor how this component interacts with the genetic changes to produce T1D.
This study is the first attempt at integrating and analyzing the intersection of genetics and environment to determine not only the relationship but also the mechanism by which these two factors conspire to induce T1D in children. This alone makes the work highly innovative. By better understanding these interactions, one can envision new and novel approaches to correcting the disease by introducing specific DNA modifications of beta cells grown in culture prior to their reintroduction in the patient, making these cells resistant to subsequent environmental triggers and interactions with the immune system.