It is generally believed that an effective cure for type 1 diabetes will require two substantial scientific advances. First, in order to restore the pancreas' ability to produce insulin, new islet beta cells must be provided, either by transplanting cells from a healthy donor or by encouraging the growth and/or function of the diabetic patient's own cells. Second, to protect the new beta cells, no matter what their origin, it is necessary to repair the breakdown in immunological tolerance that precipitated the anti-islet attack in the first place.
In a widely discussed paper that appeared in Science in 2003, Dr. Denise Faustman and her colleagues reported successful achievement of both of these advances, resulting in the "cure" of a substantial fraction of severely diabetic NOD mice, the most popular animal model of human type 1 diabetes. Their method entailed giving diabetic mice a temporary islet transplant from a genetically identical mouse, administering a single injection of an immuno-stimulatory compound called Complete Freund's Adjuvant (CFA), and repeatedly injecting a large number of spleen cells taken from genetically different mice. It was thought that the islets served to keep the animals with diabetes healthy long enough for the other treatments to have their effects, that the CFA eliminated the autoimmune attack on the islets, and that the spleen cells somehow gave rise to insulin-producing cells, presumably beta-cells, ultimately leading to islet regeneration.
"The compound CFA has been used to modulate diabetes in NOD mice for a number of years in a variety of experimental contexts, so its effect was not very surprising. However, the notion that adult spleen cells from one mouse could give rise to new islets in the pancreas o