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Defeat Diabetes: Researchers Move One Step Closer To A Cure -
Researchers Move One Step Closer To A Cure -
Type 1 Diabetes

posted 05/23/03

Medicine has 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.

The traditional therapy for type 1 diabetes involves administering insulin - usually by injection - after 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 2003 issue of the journal Diabetes, the team lead by David Serreze, PhD, a senior staff scientist at the Jackson Laboratory, reported that diabetes development is inhibited in nonobese 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 beta 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 beta cells resistant to the autoimmune processes that cause their destruction in people with type 1 diabetes, as well as in the NOD mouse model," said Serreze. "The trick was to make NOD beta cells express genes that adenoviruses normally use to protect themselves against immunological recognition.

Source: Diabetes News: This article was prepared by Immunotherapy Weekly editors from staff and other reports.

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