The actual cause of type 1 diabetes has always been a puzzle. One piece may now have been identified.
Researchers from the University of Colorado have identified a new class of antigens that may be a trigger for type 1 diabetes.
Type 1 diabetes is an autoimmune disease, in which the immune system attacks the body's own tissues. In type 1 diabetes, that attack centers on the beta cells in the pancreas.
Beta cells produce insulin, the hormone that regulates blood sugar. Without insulin, the blood sugar just keeps rising. Untreated type 1 diabetes is invariably fatal and there is no known cure.
Type 1 diabetes may result from an infection or other environmental triggers, according to the US National Library of Medicine. The infection produces molecules called antigens that cause the body to start destroying its own tissue.
Study author Kathryn Haskins, PhD, said in a press release, "Our lab studies the type of T cell known as a CD4 T cell. We have focused on autoreactive CD4 T cells using a mouse model of autoimmune diabetes. We have been especially interested in identifying the antigens that activate these T cells."
Dr. Haskins is a professor of immunology and microbiology at the University of Colorado.
T cells are part of the autoimmune system. They attack and destroy foreign molecules that enter the body as a result of a cut or infection.
In type 1 diabetes, the T cells attack beta cells instead. If researchers can identify the antigens that trigger the T cells, they may also be able to use them to turn off the T cells and prevent the disease.
Using mice with type 1 diabetes, Dr. Haskins and colleagues analyzed beta cells to find CD4 T cell antigens.
They discovered a new class of antigens consisting of fragments of insulin fused to proteins in the beta cells. Since these fused antigens aren't normal, the body doesn't recognize them and attacks.
In addition to helping scientists understand diabetes, this new discovery may shed light on other autoimmune diseases like rheumatoid arthritis.
The study was published in the February issue of Science.
Study funding was provided by the National Institutes of Health, an American Diabetes Association, the Australian National Health and Medical Research Council, and others.
Information on conflict of interest was not available.
