Germs may play a role in the development of type 1 diabetes by triggering the body’s immune system to destroy the cells that produce insulin, new research suggests.
Scientists have previously shown that killer T-cells, a type of white blood cell that normally protects us from germs, play a major part in type 1 diabetes by destroying insulin producing cells, known as beta cells.
Now, using Diamond Light Source, the UK’s synchrotron science facility, to shine intense super powerful X-rays into samples, a team from Cardiff University found the same killer T-cells that cause type 1 diabetes are strongly activated by some bacteria.
The team hopes this research will lead to new ways to diagnose, prevent or even halt type 1 diabetes.
“Killer T-cells are extremely effective at killing off germs, but when they mistakenly attack our own tissues, the effects can be devastating,” said Cardiff University’s Professor Andy Sewell, lead author of the study.
“During type 1 diabetes, killer T-cells are thought to attack pancreatic beta cells. These cells make the insulin that is essential for control of blood sugar levels.
“When beta cells are destroyed, patients have to inject insulin every day to remain healthy,” said Sewell.
Unlike type 2 diabetes, type 1 diabetes is prevalent in children and young adults, and is not connected with diet.
There is little understanding of what triggers type 1 diabetes and currently no cure with patients requiring life-long treatment.
“Killer T-cells sense their environment using cell surface receptors that act like highly sensitive fingertips, scanning for germs,” said Dr David Cole from Cardiff University.
“However, sometimes these sensors recognise the wrong target, and the killer T-cells attack our own tissue. We, and others, have shown this is what happens during type 1 diabetes when killer T-cells target and destroy beta cells.
“We identified part of a bug that turns on killer T-cells so they latch onto beta cells. This finding sheds new light on how these killer T-cells are turned into rogues, leading to the development of type 1 diabetes,” said Cole.
The research, published in The Journal of Clinical Investigation, provides a first ever glimpse of how germs might trigger killer T-cells to cause type 1 diabetes, but also points towards a more general mechanism for the cause of other autoimmune diseases.
“We still have much to learn about the definitive cause of type 1 diabetes and we know that there are other genetic and environmental factors at play.
“This research is significant as it pinpoints, for the first time, an external factor that can trigger T-cells that have the capacity to destroy beta cells,” Cole added.