Andrew Lee

2007 Research Trainee Award, Junior Graduate Studentship

The role of toll-like receptors in autoimmunity in non-obese diabetic mice|,|

More than 180 million people worldwide have either type 1 or type 2 diabetes. People with this condition are unable to maintain normal blood sugar levels due to a lack of, or insensitivity to, insulin, a hormone that regulates blood sugar levels. Whereas type 2 diabetes is usually caused by eating an unhealthy diet, type 1 diabetes is an autoimmune disease in which the affected person’s own immune system destroys the insulin-producing islet cells in the pancreas.

Research shows that killer T cells (immune cells that normally attack virus-infected cells) cause type 1 diabetes by destroying islet cells. However, there has been little research completed to date regarding what causes T cells to attack the body’s cells. It has been hypothesized that sensors that recognize microbes like bacteria and viruses, called TLRs (toll-like receptors), may play a role. TLRs activate the immune system to fight off microbes; however, TLRs are also suspected of playing a role in the onset of type 1 diabetes.

Andrew Lee is investigating whether a group of TLRs activate or accelerate the destruction of healthy cells in autoimmune diseases. Lee will also determine whether older, anti-malaria drugs and new designer DNA drugs can block these TLRs. Since symptoms of type 1 diabetes only appear when the pancreas is irreversibly damaged, this research could be used to identify people at risk of developing type 1 diabetes, and lead to new ways of preventing and treating the disease.

Completed award term, March 2009

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