For researchers, one of the most frustrating things about type 1 diabetes is that they haven’t been able to determine exactly what causes it. We know that the body’s immune system mistakenly causes T cells in the pancreas to destroy insulin-producing beta cells — but why?
In a groundbreaking article just published in the journal Science Immunology, scientists from Scripps Research, a California-based biomedical research facility, said that they have found a switch that causes the immune system to begin destroying beta cells. For more than five years, they ran a series of experiments on nondiabetic, overweight mice that they judged to be in a prediabetic state. They sequenced T cells from their blood and analyzed the vast amount of data they collected.
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The researchers were able to uncover a mechanism that they call the “P9 switch.” The switch allowed a particular group of T cells to attack the islet cells. The researchers also found that the cells turned on by the switch lasted a very short time — the cells initiated a bout of cell destruction and then vanished. The Scripps researchers conjectured that it was because the cells’ lifespans were so brief that previous diabetes researchers had been unable to identify them.
The researchers hypothesize that immune cells containing the P9 switch would be detectable only in those who are in the early stages of developing type 1 diabetes.
They plan, therefore, to recruit 30 people who are considered to be at risk of developing the disease and collect blood samples to see if they contain the P9 switch. If they find that a blood test can demonstrate the presence of the switch-bearing cells, the discovery could lead to extremely early detection of type 1 diabetes and thus enable early intervention and perhaps even a method of blocking the development of the illness. As research team leader Luc Teyton, MD, PhD, explained, “The translational aspect of this study is what’s most exciting to me. By using single-cell technologies to study the prediabetic phase of disease, we have been able to mechanistically link specific anti-insulin T cells with the autoimmune response seen in type 1 diabetes. And that has given us the confirmation we needed to move into human studies.”
A freelance writer and editor based in the Chicago area, Gustaitis has a degree in journalism from Columbia University.