US scientists have proposed an alternative theory about the cause of type 1 diabetes, which could open up new research options into the condition.
It has been long understood that the root cause of type 1 diabetes was the immune system mistakenly attacking insulin-producing beta cells.
But scientists at the City of Hope’s Diabetes and Metabolism Research Institute say that it is actually these beta cells that cause this immune response.
“Our findings show that type 1 diabetes results from a mistake of the beta cell, not a mistake of the immune system,” said lead researcher Bart Roep, Ph.D.
“The immune system does what it is supposed to do, which is responding to distressed or ‘unhappy’ tissue, as it would in infection or cancer.”
Roep and colleagues made this discovery upon examining cancer molecules that are targeted by the immune system following immunotherapy.
They discovered a protein error in this sequence that is also produced by the beta cells in people with type 1 diabetes, and believe this “wrong read” also occurs with the insulin gene, making it a major target of the immune system.
Significantly, Roep and colleagues believe this ‘wrong read’ of the insulin gene occurs when beta cells are stressed.
“Our study links anti-tumour immunity to islet autoimmunity, and may explain why some cancer patients develop type 1 diabetes after successful immunotherapy,” added Roep. “This is an incredible step forward in our commitment to cure this disease.”
“[Our findings] further support the emerging concept that beta cells are destroyed in T1D by a mechanism comparable to classical antitumor responses where the immune system has been trained to survey dysfunctional cells in which errors have accumulated.”
Last month the City of Hope was given a £40m grant to cure type 1 diabetes within six years.
As part of this ongoing research, Roep’s team will now look to correct the autoimmune response against beta cells and prevent the development of type 1 diabetes.
The study has been published online in the journal Nature Medicine.

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