Scientists have solved a decades-old medical mystery by finally identifying a previously unknown molecule which is attacked by the immune system in people with Type 1 diabetes.
The ground-breaking research, led by Dr Michael Christie from the University of Lincoln, UK, could now lead to better identification of individuals at risk of Type 1 diabetes and inform the development of new therapies which could prevent the disease developing.
Type 1 diabetes develops when the body is unable to produce insulin; a substance required to regulate blood sugar levels by moving glucose out of the blood and into cells to be used for energy.
It is an autoimmune disease, where the body’s defense system that normally protects against infections attacks and destroys the insulin-producing cells in the pancreas.
In Type 1 diabetes, the immune system reacts to particular molecules in the pancreas — called autoantigens — that it would normally ignore.
People with Type 1 diabetes have antibodies in their blood that are specific to each of the molecules.
Tests are currently used to detect these antibodies: the more antibodies detected, the higher the risk a person has of developing Type 1 diabetes.
The tests are currently used to identify those most at risk of Type 1 diabetes, and in the future could provide an opportunity to intervene and stop the disease in its tracks.
Until now, scientists had found four molecules that are attacked by the immune system in Type 1 diabetes.
The identity of a fifth molecule — known only as ‘Glima’ for the past 20 years — has been a mystery.
Dr Christie’s team have successfully identified this fifth molecule as Tetraspanin-7, which could make tests for predicting Type 1 diabetes more accurate.
They are now searching for ways to block the immune attack, in order to prevent Type 1 diabetes from developing in those at a high risk.
The research was funded by Diabetes UK and the Society for Endocrinology and is published in Diabetes, the journal of the American Diabetes Association.
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News source: University of Lincoln. The content is edited for length and style purposes.
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