Scientists in Japan have found a way to improve on a promising diabetes treatment. In the October 3 issue of The Journal of Experimental Medicine, Masaru Taniguchi and colleagues report that transplanted insulin-producing cells survive better when the activation of a specific type of immune cell is blocked.
Insulin-dependent diabetes is caused by the destruction of the insulin-producing cells in the pancreas (called islet cells) by auto-reactive T cells. The loss of insulin results in an inability to control blood sugar levels. Transplantation of islet cells is an effective way to restore insulin production, but this therapy requires life-long immunosuppression of the patient. Even with immunosuppression, up to half of the transplanted cells are rapidly destroyed by the patients own T cells.
Taniguchis group used a mouse model to show that a subset of cells known as natural killer T (NKT) cells instigates the rapid destruction of the islet cells. NKT cells become activated -- likely in response to the stress of the transplant procedure -- and produce an inflammatory molecule called interferon (IFN)-gamma, which helps to activate the auto-reactive T cells. In mice that lack NKT cells or are unable to produce IFN-gamma, the transplanted cells survived.
Nickey Henry | EurekAlert!
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