Scientist are still unsure as to why the body's immune system attacks part of its own pancreas, better known as Type 1 diabetes, a chronic autoimmune disease. However, they might have a much better understanding now as to how this disease can cause such a ruckus in the human body. Scientist have long known that the disease attacks four molecules which is known as autoantigens, located in the pancreas. Now, they have recently discovered that a fifth molecule might just also be under attacked.
The fifth and final molecule, now identified as tetraspanin-7, was recently discovered by U.K. and Italian researchers. Because of their discovery, the future of predicting diabetes and further bettering diabetic treatment will be much easier.
“The discovery that tetraspanin-7 is a major target of immunity in diabetes now provides us with a complete picture of what the immune system recognizes in individual patients, will assist in identifying individuals at risk through detection of antibodies to the protein and will allow the development of procedures to block the tetraspanin-7 immune response as part of a strategy to prevent the disease,” said Dr. Michael Christie, lead researcher at the University of Lincoln.
The way to identify diabetes is based on the levels of sugar in the blood. The body is not capable of producing enough insulin. 1.25 million Adults and children are diagnosed with Type 1 diabetes just in the U.S. alone. Insulin is a hormone that helps distribute sugar found in the blood to other parts of the human body.
Diabetes is commonly treated with insulin for those suffering or have developed Type 1 diabetes. Ways of getting insulin into the body is through injection or through a pump. To check their glucose level, they would need to prick their finger and check it with a blood sugar monitor. However, even with insulin, they still will experience many complications that affect their nervous system, feet, eyes and circulation.
"The discovery that tetraspanin-7 is a major target of immunity in diabetes now provides us with a complete picture of what the immune system recognizes in individual patients...” said Christie.
After analyzing Type 1 diabetic blood samples from different patients, researchers learnt to identify the molecules by using the antibodies that were linked to tetraspanin-7. They were successful in binding the antibodies to tetraspanin-7.
“We were surprised that we were finally able to discover the identity of the target of antibodies in Type 1 diabetes after such a long period, with many groups worldwide on the hunt for it during this time,” Christie said. “We almost gave up at one stage — our initial test for binding of patients’ antibodies to tetraspanin-7 was negative! — but we then realized that perhaps the test we were using was flawed, so we tried a different approach which worked nicely.”
Dr. Emily Burns co-funded the groundbreaking study along with the Society of Endocrinology.
“In order to prevent Type 1 diabetes, we need to fully understand how the immune response that damages insulin-producing cells develops in the first place,” she said. “Dr. Christie’s impressive research is helping us to do just that.”