University of Pittsburgh researchers have figured out how to prevent type 1 diabetes in mice, with the hope of eventually preventing it in people.

But application to humans remains a distant goal.

Dr. William M. Ridgway, a doctor and assistant professor at the University of Pittsburgh School of Medicine's Department of Rheumatology and Clinical Immunology, said three years of research succeeded in preventing diabetes in mice.

Another focus is identifying the configuration of genes in mice that renders them vulnerable to the chronic condition, with hopes of defining what genes make people susceptible to the disease.

Such research is important in identifying people with a genetic predisposition for diabetes as a first step in preventive action, Dr. Ridgway said.

The Pitt research team has identified an antibody that activates immune cells, known as regulatory T-cells, and prevents rogue auto-reactive T-cells, which cause autoimmune diseases, from destroying insulin-producing beta cells in the pancreas of mice. As a result, mice are protected from diabetes.

The study is published this month in "Diabetes," a research journal of the American Diabetes Association.

Many aspects of the autoimmune process remain unclear, but Dr. Ridgway said the research sheds light on why immune cells can go awry and attack good cells in diseases like diabetes.

"This was confusing, and it took time to unravel it, and we're excited to see the results," he said. "It's important research, but we still have a long way to go to unravel those things."

More than 700,000 Americans have type 1 diabetes, an autoimmune disorder in which the body errantly attacks insulin-producing cells of the pancreas. The attack reduces or eliminates one's ability to produce insulin, a hormone necessary to convert blood glucose into energy.

The resulting buildup of blood glucose, if not controlled, can lead to blindness, kidney failure, heart disease, nerve damage and other medical problems.

Treatment is a balancing act. Type 1 diabetics must take daily doses of insulin and follow a strict diet to control blood-glucose levels. The diabetic also must test blood glucose regularly to prevent high readings that cause long-term health problems and low readings that require consumption of sugar to prevent weakness, sweating, confusion and eventually unconsciousness and even death.

The Pitt research focuses on T-cells, receptors and antibodies in the immune system and provides a new understanding of why T-cells, which are supposed to destroy infections and pathogens in the blood, become turncoats and kill insulin-producing cells they're supposed to protect.

Two types of T-cells are involved in diabetes -- turncoat auto-reactive T-cells, or T-cells gone bad, that kill the insulin producing cells, and regulatory T-cells that are unable to control the auto-reactive T-cells.

In diabetics, Pitt research concludes, the regulatory T-cells are faulty or lacking in number, which allow auto-reactive T-cells to destroy islet cells that produce insulin.

But Dr. Ridgway said his team used an antibody to activate the regulatory T-cells through the CD137 receptor on the cells, which boosts the number and function of the cells so they can counter the auto-reactive T-cells.

"Think of it as a war between regulatory T-cells and pathogenic T-cells," he said. "The antibody boosts the powers of the good, regulatory cells."

A future goal is to determine whether the same biology occurs in humans, and whether an antibody can be used in humans to boost good regulatory T-cells.

Dr. Ridgway said his team is working to identify the combination of genes in mice that renders them vulnerable to diabetes. If that "bad hand" of genetic cards can be determined in people, it could be used to identify who should undergo preventive therapy.

The National Institutes of Health funded the study through the Autoimmunity Center of Excellence at Pitt headed by Dr. Massimo Trucco, a doctor and diabetic researcher.

The research team included three other Pitt Medical School researchers -- Junichiro Irie, Yuehong Wu and Kritika Kachapati -- and Dr. Robert S. Mittler of the Department of Surgery at Emory Vaccine Center, Emory University School of Medicine, Atlanta.

"If we can demonstrate this same genetic predisposition and therapeutic effect in human type 1 diabetes patients, then this may prove to be a significant step toward preventing this disease before it can take hold," Dr. Ridgway said.