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FRIDAY, May 16 (HealthDay News) -- New details about the immune cells thought to be responsible for type 1 diabetes are revealed in a study by scientists at Washington University School of Medicine in St. Louis.
In research with diabetic mice, the scientists found these dendritic cells in insulin-making structures in the pancreas called the islets of Langerhans and observed them carrying insulin and fragments of insulin-producing cells known as beta cells. This can be the initial step toward the start of a misdirected immune system attack that destroys the beta cells and prevents the production of insulin, resulting in type 1 diabetes.
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The findings may help in efforts to develop ways to treat type 1 diabetes, the researchers said. An estimated 1 million to 2 million Americans have type 1 diabetes, according to the American Diabetes Association.
"Now that we've isolated dendritic cells from the pancreas, we can look at why they get into the pancreas and determine which of the materials that they pick up are most critical to causing this form of diabetes. That may allow us to find ways to inhibit dendritic cell function in order to block the disorder," study senior author Dr. Emil R. Unanue, a professor of pathology, said in a prepared statement.
The study was published online in this week's issue of the Proceedings of the National Academy of Sciences.
In a separate line of investigation, researchers in Unanue's lab found that dendritic cells in the pancreas may normally have beneficial effects on the health of beta cells. The team found that when there are no dendritic cells in the pancreas, beta cells are smaller, a sign that they're not as healthy.
"We think these dendritic cells aren't in the pancreas by accident. We believe that, in the normal individual, they help maintain the health of beta cells. But in a person with autoimmune diabetes, they appear to start the problems that destroy beta cells," Unanue said.
More information
The American Academy of Family Physicians has more about type 1 diabetes.
-- Robert Preidt
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