Scientists take big step in better understanding Type 1 diabetes
27 Apr 2016
Scientists have taken a big step in better understanding how Type 1 diabetes wreaked havoc on the body, which could lead to novel treatments for the disease.
It was known that in the chronic autoimmune disease the immune system attacks four molecules, called autoantigens, in the pancreas. However, there had been much speculation in medical circles about a fifth molecule that was also under attack, but which remained unidentified it until now.
Researchers in the UK and Italy have identified the fifth and final molecule, called tetraspanin-7. According to Dr Michael Christie, reader in biomedical sciences at the University of Lincoln in England who led the research, their work could improve diabetes prediction and treatment.
''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,'' Christie told The Huffington Post yesterday.
People with diabetes have high levels of sugar in the blood as the body failed to produce any or enough insulin, a hormone that helped to take sugar from the blood to other parts of the body.
In Type 1 diabetes, the immune system destroyed the beta cells that make insulin.
Christie told the BBC, "With this new discovery, we have now finished identifying what the immune system is targeting - we have the complete picture."
The targets are:
- Insulin
- Glutamate decarboxylase
- IA-2
- Zinc transporter-8
- And the final piece of the puzzle, tetraspanin-7
According to Christie having the complete picture could help transform care for type 1 patients.
He said, "Once the immune system decides it wants to get rid of something it's very hard to stop, so diabetes has proved to be a difficult disease to prevent.
"So we're hoping that, by having identified the major targets in the disease, we can find ways to prevent it by blocking the immune response to these five proteins without leaving that person vulnerable to infections.
"With recent improvements in our understanding of the disease I'm very hopeful we'll develop a treatment now; I have a lot more confidence than even five years ago."
