Scientists at the Stanford University School of Medicine and the University of Toronto have showed that type 2 diabetes could derive from an autoimmune reaction from within the body. It is hoped the breakthrough will lead to new therapies for treating the condition.
The research, published in the journal Nature Medicine, found that an antibody called anti-CD20 was effective in treating laboratory mice with type 2 diabetes . Although more work is needed to test it on humans, the anti-CD20 can pinpoint and eliminate mature B cells, which could prevent the development of type 2 diabetes in those prone to the condition, as well as helping to replenish their blood sugar .
A human version of anti-CD20, which is already used for treating some blood cancers and autoimmune diseases in humans, is called rituximab, is available under the trade names of Rituxan and MabThera. It is thought that insulin resistance comes about when the B cells and other immune cells react against tissues in the body.
Daniel Winer, senior author on the study, commented “We are in the process of redefining one of the most common diseases in America as an autoimmune disease, rather than a purely metabolic disease.”
He added “This work will change the way people think about obesity, and will likely impact medicine for years to come as physicians begin to switch their focus to immune-modulating treatments for type 2 diabetes.”

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