Researchers Move One Step Closer to Curing Type 1 Diabetes

Date: April 25, 2003

Bar Harbor, Maine-Medicine moved a bit closer to curing a form of diabetes by learning how to make a body accept the insulin producing cells it once destroyed.

In type 1 diabetes, a patient's defense system goes awry and attacks the cells that produce insulin. The immune system mistakes the individual's insulin-producing cells, found in a part of the pancreas, for a foreign protein and destroys them. The traditional therapy involves administering insulin-usually by injection -once the patient loses the ability to make enough to regulate blood sugar levels. Recent attempts to graft cells from a healthy pancreas to diabetic patients show promise, but require powerful immunosuppressive drugs to prevent a repeat of the immune response that precipitated the condition. Yet drugs that diminish a person's ability to attack foreign proteins carry a high price in risk of disease and infection.

Scientists at The Jackson Laboratory, in conjunction with collaborators at the Albert Einstein College of Medicine, discovered a way to protect insulin producing cells from the immune responses that cause type 1 diabetes. A family of viruses, originally identified in human adenoid tissue, cause respiratory diseases. These adenoviruses make several proteins that thwart the immune process from destroying them, without diminishing the system's ability to fight other invaders.

In an article in the May issue of the journal Diabetes, the team lead by David Serreze, Ph.D., a senior staff scientist at The Jackson Laboratory, reported that diabetes development is inhibited in non-obese diabetic mice that have been genetically engineered to express adenovirus-derived immunological shielding proteins in insulin producing cells of the pancreas. Their findings might ultimately lead to a way that would protect engrafted pancreatic ß cells from being destroyed by the immunological processes that cause type 1 diabetes, and thus allow them to reverse disease without putting patients on immunosuppressive drugs.


"We found a trick that makes insulin producing pancreatic ß cells resistant to the autoimmune processes that cause their destruction in people with type 1 diabetes, as well as in the NOD mouse model," says Dr. Serreze. "The trick was to make NOD ß cells express genes that adenoviruses normally use to protect themselves against immunological recognition.

"Our findings might ultimately lead to a way that would protect engrafted pancreatic ß cells from being destroyed by the immunological processes that cause type 1 diabetes, and thus allow them to reverse disease without putting the patient on immunosuppressive drugs," Dr. Serreze notes.

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Adenovirus Early Region 3 Antiapoptotic 10.4K, 14.5K,and 14.7K Genes Decrease the Incidence of Autoimmune Diabetes in NOD Mice. Diabetes, Vol. 52, May 2003. Melissa A. Pierce, Harold D. Chapman, Cristina M. Post, Anton Svetlanov, Shimon Efrat, Marshall Horwitz (Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York) and David V. Serreze.

Contact(s): Joyce Peterson, 207-288-6058, joyce.peterson@jax.org

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