Scientists in Japan have found a way to improve on a promising diabetestreatment. In the October 3 issue of The Journal of ExperimentalMedicine, Masaru Taniguchi and colleagues report that transplantedinsulin-producing cells survive better when the activation of aspecific type of immune cell is blocked.
Insulin-dependent diabetes is caused by the destruction of theinsulin-producing cells in the pancreas (called islet cells) byauto-reactive T cells. The loss of insulin results in an inability tocontrol blood sugar levels. Transplantation of islet cells is aneffective way to restore insulin production, but this therapy requireslife-long immunosuppression of the patient. Even withimmunosuppression, up to half of the transplanted cells are rapidlydestroyed by the patient's own T cells.
Taniguchi's group used a mouse model to show that a subset of cellsknown as natural killer T (NKT) cells instigates the rapid destructionof the islet cells. NKT cells become activated -- likely in response tothe stress of the transplant procedure -- and produce an inflammatorymolecule called interferon (IFN)-gamma, which helps to activate theauto-reactive T cells. In mice that lack NKT cells or are unable toproduce IFN-gamma, the transplanted cells survived.
The group went on to show that multiple doses of a drug (calledalpha-galactosylceramide), which activates NKT cells in single doses,caused these cells to produce less IFN-gamma. The decreased IFN-gammaproduction protected the transplanted islet cells. The authors thussuggest that multiple doses of the same compound, currently in clinicaltrials in humans, might help prevent the early loss of transplantedislet cells in patients with insulin-dependent diabetes.
Materials provided by Journal of Experimental Medicine. Note: Content may be edited for style and length.
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