Cure Research Back in the News

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Jun 1, 2006

Two and a half years ago, the journal Science published results from Denise Faustman’s groundbreaking study in which type 1 diabetes was reversed in non-obese diabetic mice injected with a combination of an immune adjuvant and spleen cells. Recently, researchers at the University of Chicago, Washington University in St. Louis and Harvard’s Joslin Clinic all partially replicated Dr. Faustman’s research.

In the March 24 issue of Science, it was reported that severely diabetic mice may be able to recover on their own when injected with an immune adjuvant called Freund’s complete adjuvant, which consists of a mixture of water, oil and parts of dead bacteria. In her March 24, 2006, column for The New York Times, science writer Gina Kolata writes that this immune adjuvant “overstimulates the immune system cells that are attacking the pancreas, making those white blood cells self-destruct, effectively stopping the attack and allowing the pancreas to cure itself.”

According to the latest Science studies, simple injection of the immune adjuvant alone cured type 1 in 32 percent of the non-obese diabetic mice. Faustman’s earlier theory was that injecting the immune adjuvant with spleen cells helped reverse type 1 in the mice.

Science, March 24, 2006

The New York Times, March 24, 2006

Anita S. Chong, PhD, associate professor, Section of Transplantation, in the Department of Surgery at the University of Chicago, was a lead researcher on the Science study:

Q: How is this research significant in the search for a type 1 cure?

A: It emphasizes that diabetic mice with a substantial loss in beta cells can still regenerate sufficient beta cell mass under conditions when the autoimmune attack is controlled and the blood glucose levels are normalized (in this case, with a temporary islet transplantation).

Q: How much of a departure is this from Denise Faustman’s November 2003 discovery?

A: There is a significant departure, because Denise had claimed in the 2003 paper that there were stem cells in the spleen that could morph into beta cells, thus raising the possibility of a new source of beta cells that can be used to replace beta cells that had been destroyed in type 1 diabetics. All three groups in the recent Science articles were not able to demonstrate a contribution of spleen-derived beta cells in the mice with regenerated beta cell function.

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