Research by Dr Robyn Slattery, from the John Curtin School of Medical Research in Canberra, has shed important light on the process by which type 1 diabetes is initiated.

In a paper* published in the Proceedings of the National Academy of Sciences (PNAS) journal, Dr Slattery has announced that while interaction between T Cells and beta cells in the pancreas is a critical step in the onset of type 1 diabetes, it does not initiate the disease process.

This paper was cited third in the recent "Trends in Immunology" journal, which discusses a paradigm shift in the way scientists look at the cause and early progression of type 1 diabetes.

We know that in type 1 diabetes, the immune system mistakenly turns on itself, destroying the beta cells within the pancreas and removing the body's ability to produce the hormone insulin. Insulin allows the body to process sugar to create energy.

In the past, many researchers believed that there must be direct interaction between specific T cells (called CD8 T cells) and a particular marker on the beta cells (called MHC class I) for the process that causes the destruction of beta cells to start and for the early progression of disease known as insulitis.**

This research reveals that this belief is in fact incorrect. Dr Slattery's findings will have an important influence on the direction of future research into understanding the early events that precede beta cell destruction and therefore help advance our understanding of how to design prevention strategies.

Dr Slattery conducted an experiment using specially bred diabetic mice that had no beta cell class I expression. Despite the absence of this molecule (which is required for CD8 killer T cells to act), both the initiation and progression of insulitis still occurred. This demonstrates that direct interaction between CD8 T cells and beta cells is not required for initiation or early progression of type 1 diabetes.

Without beta cell class I expression, however, the vast majority of the mice did not go on to develop high blood glucose levels. This indicates that this step is still required for type 1 diabetes to occur. Hence, the requirement for class I on beta cells is a relatively late checkpoint in the development of diabetes.

This research was funded by the Juvenile Diabetes Research Foundation (JDRF Research Grant, 1 April 2000 - 31 March 2003, US$329,484)

The innovative nature of Dr Slattery's research and her promising results has led JDRF to award her a further three year research grant (US$495,000 1 April 2003 - 31 March 2006). Dr Slattery's world leading research utilizes highly sophisticated new genetic techniques to help understand the causes of type 1 diabetes. Dr Slattery was responsible for discovering the first diabetes susceptibility gene in mice in 2001.

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* Dr Slattery's paper is titled "Beta cell MHC class I is a late requirement for diabetes" and was published in May 2003.
** Insulitis is the invasion of the pancreatic islets by lymphocytes. This produces an autoimmune response which leads to destruction of the beta cells.

JDRF is the leading non-profit funder and advocate of type 1 (juvenile) diabetes research worldwide. It was founded in 1970 by the parents of children with juvenile diabetes - a disease which strikes children suddenly, makes them insulin-dependent for life, and carries the constant threat of devastating complications. Since inception, JDRF has provided more than US$600 million in direct funding to diabetes research. JDRF's mission is constant: to find a cure for diabetes and its complications through the support of research.

For further information:

Karolyn Andrews, Media & PR Manager, JDRF
Ph. 02 9966 0400 (x203) or 0403 787 077 | email: kandrews@jdrf.org.au