Why WBCs Attack Beta Cells in Type 1 Diabetes

by Mark Benson on March 13, 2012

Immune system triggered to attack islet cells

According to a new research from the Juvenile Diabetes Research Fund, many genes that influence Type 1 diabetes are also found in pancreatic beta cells. This finding suggests that insulin-producing cells play a role in why white blood cells attack, thus leading to Type 1 diabetes.

The study was published in the March issue of PLoS Genetics, the research was conducted in Belgium finding that after extensive research and cataloguing of 15,000 genes expressed in human islet cells, it reached a conclusion that the beta cells themselves contribute to their demise leading to Type 1 diabetes.

The research head is Decio Eizirik MD, PhD, a professor and current Director of the Laboratory of Experimental Medicine at the Universite Libre de Bruxells located at Brussels, Belgium. The team utilized the technique called RNA sequencing where the process identifies all the forms of transcribed RNAs in a particular cell. The aim is to assemble a catalog that showed more than 15,000 genes that are expressed in healthy beta cells. The transcribed RNA molecules then serve as the means wherein the genetic information is expressed.

The researchers observed that many of the known genes related to Type 1 diabetes are also present in human islet cells. When these very same cells are exposed to cytokines, which are released by immune cells, these trigger the onset of diabetes. It was also noted that there are changes in the expression patterns in these genetic structures. This observation leads the researchers to the conclusion that the islets themselves are contributory to the recruitment of immune cells when Type 1 diabetes begins to develop. As this occurs, the immune system attacks these beta cells, leading to their demise and development of type 1 diabetes.

According to Dr. Eizirik, “Based on our research, our understanding now is that Type 1 diabetes in its early stages, is characterized by a dialog between beta cells and the immune system, instead of the previous view of beta cells as purely passive victims of the immune attack. We can now open our eyes a bit wider to the possible ways that Type 1 diabetes can develop. As we expand our focus on beta cells, we could start to unearth more answers in the mystery of this disease.”

Julia Greenstein, PhD added, “What we’re seeing is that beta cells may in fact be playing a larger role in triggering Type 1 diabetes than we previously thought and exploring this concept more deeply could lead to a better understanding of the what causes the autoimmune attack. Dr. Eizirik’s work is important to JDRF because it shows us that there is a need for more research on beta cell survival and health and its role as a potentially key part of the early disease process. Furthermore, the catalog of genes from this study will continue to support progress in many more areas of diabetes research.”

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