Researchers have discovered the last piece of the puzzle of which regions the body’s own immune system attack during type 1 diabetes. After almost two decades of searching, the entire picture of how the condition causes the destruction of the insulin-producing cells in the pancreas is now clear. It seems that along with four other parts of the cells, the immune system also targets a specific protein that is involved in the growth and development of the beta cells.
Now that researchers have this overarching view of the exact bits of the cells the antibodies target, it could open up new avenues for treatments for the condition. “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,” Dr. Michael Christie, who led the research published in the journal Diabetes, told BBC News.
"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.”
By looking at the antibodies produced by the immune system when it launches its attack during type 1 diabetes, scientists had realized that there were five different types, meaning that it was targeting five different aspects of the beta cells. The antibodies eventually cause the destruction of these cells, which are responsible for the production of insulin, and leads to high levels of glucose in both the blood and urine. The main tests for type 1 look for these antibodies to be present.
Yet what exactly these antibodies target on the beta cells hasn’t been completely clear. Researchers had managed to work out what four of these marks were – insulin, glutamate decarboxylase, IA-2, and zinc-transporter-8 – but the fifth target has remained elusive, until now. “With this new discovery, we have now finished identifying what the immune system is targeting – we have the complete picture,” explained Dr. Christie.
They have found out that the final piece of the puzzle is made from cell-surface protein called “tetraspanin-7,” and plays a key role in cell development, growth, and motility. By finally understanding the full picture of which aspects the immune system is attacking, researchers might be able to come up with novel ways to either stop, or at least stall, the development of type 1.
Hopefully, further research can be carried out not only in how better to identify those at risk of the condition, but even to try and prevent or stop it in the first place.
