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Insulin Triggers Autoimmune Response In Diabetes

  May, 17 2005 9:54
your information resource in human molecular genetics
For many years, scientists have struggled to understand what causes the body to turn against itself in Type 1 diabetes, a disease affecting about one in every 400-500 children and adolescents in the United States. In this disease, the immune system destroys pancreatic cells that normally produce the blood-sugar-regulating hormone insulin. Now, two papers appearing in the 12 May 05 issue of Nature (Vol. 435, No. 7039, pp. 220-223 & pp. 224-228) provide convincing proof that insulin itself initiates this devastating autoimmune response.

In one paper, George Eisenbarth and his colleagues used mice that usually develop type 1 diabetes and engineered them to lack normal insulin. To make sure the animals did not die, researchers designed them to carry a form of insulin that was hormonally active but not recognized by immune cells. The mice with this modified insulin did not develop diabetes.

Results presented by David Hafler and his fellow researchers support the idea that insulin has an essential role in this autoimmune response in humans. The scientists isolated immune cells from the pancreatic draining lymph node of patients with type 1 diabetes and analysed the proteins that the cells recognized. In contrast with cells from healthy control subjects, half of the isolated cells from diabetics reacted to insulin protein.

"Findings - suggest that insulin could be the target of the autoimmune response in humans providing a potential candidate for treatment", writes Matthias von Herrath in a related News & Views article.


George G. S. Eisenbarth (University of Colorado Health Sciences Center, Denver, CO, USA)
E-mail: george.eisenbarth@uchsc.edu

David A. Hafler (Harvard Medical School, Boston, MA, USA)
E-mail: dhafler@rics.bwh.harvard.edu

Matthias von Herrath (La Jolla Institute for Allergy and Immunology, San Diego, USA)
E-mail: matthias@liai.org

(C) Nature press release.

Message posted by: Trevor M. D'Souza

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