Therefore, many research teams were interested in extending the potentially important findings of Dr. Faustman and her colleagues by defining the precise cellular and molecular mechanisms involved. As a necessary first step, the researchers needed to reproduce the results published in the 2003 Science paper. Unfortunately, this did not prove possible, as reported in three papers appearing in the March 24, 2006, issue of Science from groups based at Joslin Diabetes Center in Boston, Washington University in St. Louis and the University of Chicago, working entirely independently. For example, the Joslin team was not able to replicate the original findings even though it strove to match as closely as possible the published methods, and also incorporated supplementary details from more extensive protocols provided by the authors. In short, like the study of Dr. Faustman and colleagues, the three new studies resulted in a substantial fraction of severely diabetic NOD mice being "cured" of their hyperglycemia as well as their autoimmunity against beta cells. However, none of the teams found any evidence that new islet cells emanating from donor spleen cells were the source of the insulin responsible for the reversal of diabetes. Rather, even though severely diabetic, the host mice kept a substantial number of residual beta cells, and the recovered islets were all of host, rather than donor spleen cell, origin.
"Given recent reports from several groups that beta cells in adult mice can undergo active cell division, the most likely explanation for islet recovery in the 'cured' mice is that when the autoimmunity was suppressed, be