For many years scientists have known that type 1 diabetes is an autoimmune disease in which the body's immune system mistakenly launches an attack on the insulin-producing beta cells of the pancreas. At an early stage in this process, white blood cells called T-cells invade the islets of Langerhans of the pancreas, where the beta cells reside (a condition known as "insulitis"). Yet, in both mice and humans, insulitis does not always progress to full-blown type 1 diabetes. For years, researchers have been trying to determine why insulitis sometimes leads to diabetes (so-called "destructive" insulitis) and sometimes does not ("respectful" insulitis). They know that certain T-cells called T effector cells promote destructive insulitis, and other T-cells called regulatory T-cells favor respectful insulitis. Yet, no one knows exactly what causes the balance of power to shift between these two types of cells to cause diabetes.
To study this question, Anne E. Herman, Ph.D., Diane Mathis, Ph.D., and Christophe Benoist, M.D., Ph.D., of the Section on Immunology and Immunogenetics at Joslin Diabetes Center in Boston studied insulitis lesions in a certain strain of genetically engineered mice called BCD2.5 mice. These mice develop insulitis, but a very respectful form, such that diabetes does not follow until months later, or, in some, never. The researchers discovered that both effector and r
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Contact: Marge Dwyer
marjorie.dwyer@joslin.harvard.edu
617-732-2415
Joslin Diabetes Center
23-Jun-2004