November 14, 2003

Regeneration of insulin-producing islets may lead to diabetes cure

Cells from an unexpected source — the spleen — appear to develop into insulin-producing pancreatic islet cells in adult animals. This surprising finding from MGH researchers, published in the current issue of Science, describes the mechanism behind the same team's 2001 report of a cure for type 1 diabetes in mice. "We have found that it is possible to rapidly regrow islets from adult precursor cells, something that many thought could not be done," says Denise Faustman, MD, PhD, director of the MGH Immunobiology Laboratory and principal investigator. "By accomplishing effective, robust and durable islet regeneration, this discovery opens up an entirely new approach to diabetes treatment." (Faustman pictured)

In their earlier study, Faustman's team first attempted to retrain the immune system not to attack islet cells. They expected to follow that process with transplants of donor islet cells but were surprised to find that most of the mice began producing normal islets that secreted insulin. The current study showed that the new islets were regenerated from donor spleen cells, which had been administered as part of the immune-system retraining process. They also showed that islets could regrow from precursor cells that remained in the diabetic mice once the autoimmune process was halted.

David M. Nathan, MD, director of the MGH Diabetes Center, notes: "These exciting findings in a mouse model suggest that patients developing type 1 diabetes could be rescued from further destruction of their insulin-producing cells. In addition, patients with fully established diabetes possibly could have their diabetes reversed." Nathan has developed a protocol to test this approach in patients, but additional grant support is needed before a clinical trial can begin.

Faustman also hopes to investigate whether these discoveries could be applied to other autoimmune diseases, several which are believed to be caused by the same immune system disruption her team originally identified in diabetes.

Co-authors of the paper are first author Shohta Kodama, MD, PhD; Willem Kuhtreiber, PhD; Satoshi Fujimura, PhD; and Elizabeth Dale, all of the MGH Immunobiology Laboratory.