Yale discovers mechanism that explains why some beta cells survive in type 1 diabetes

Jack Woodfield
Fri, 10 Feb 2017
Yale discovers mechanism that explains why some beta cells survive in type 1 diabetes
Yale University have identified why some insulin-producing cells survive the immune attack that characterises type 1 diabetes.

The findings could lead to new strategies for saving production of these beta cells in people with type 1 diabetes, Yale researchers said.

Some beta cells can survive in people with type 1 diabetes even years after the onset of the disease, so researchers from Yale and the Broad Institute of MIT and Harvard studied changes in beta cells during immune attack in both mouse models and human cells.

"During the development of diabetes, there are changes in beta cells so you end up with two populations of beta cells," said lead author Dr. Kevan Herold.

"One population is killed by the immune response. The other population seems to acquire features that render it less susceptible to killing."

This resistant subpopulation of beta cells was observed in nine-week-old, non-obese diabetic mice. Upon detecting infiltration into the islet, the subpopulation used a "duck and cover" approach to resist immune attack.

The cells expressed molecules that inhibited the immune response, developing a stem-cell like ability to survive and even proliferate despite immune attack.

Human beta cells were shown to experience similar changes when cultured together with immune cells, and the discovery of this mechanism could impact research into type 1 diabetes treatments.

"Future studies that can recover mature [beta] cells from the pool of modified cells may identify ways of restoring normal metabolic function together with immune therapy," said the researchers.

"The next question is, can we recover these cells so that there is insulin production in someone in type 1 diabetes?" added Herold.

Herold and colleagues now plan to conduct clinical trials steered towards changing this subpopulation of beta cells into insulin-producing cells.

The findings were published in the journal Cell Metabolism.
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