Dr Hanna Skärstrand of Lund University Diabetes Centre in Malmö, Sweden, was the recent recipient of the JDRF and Macquarie Group Foundation International Diabetes Research Innovation Award. She speaks to JDRF today about her research.
My interest in human autoimmunity started during my Bachelor degree studies at Linköping University in Sweden. I was fascinated about how the immune system would attack its own tissue in a highly specific way. We now know that there is a prolonged autoimmune destruction of the insulin-producing cells prior to clinical symptom, and therefore my focus lies in the predictive aspects of the disease. It would be important to increase the knowledge about predicting the development of T1D in children with an increased risk.
While no one in my family has T1D, the disease is fairly common in Sweden compared to other countries so I do have a few friends with the disease. It was natural for me to be interested in research in this area, especially as there are still misconceptions in the public about the disease – I have often received questions about whether sweet cakes, candies and cookies will cause type 1 diabetes. I think it is very important to point out that type 1 and type 2 is two very different diseases with different complex heterogenic backgrounds.
My dissertation last year identified that a genetic mutation on a protein (known as ZnT8) changes its shape, making it easier for the ZnT8 autoantibodies to bind to the protein, which could be part of the reason for changes in the immune response. I never thought my projects would continue though, and it’s with thanks to JDRF and winning this Innovation Award that I have been able to continue with this study.
Since winning the award, we have established a new collaboration between our team of type 1 diabetes researchers at Lund University, Sweden and the Autoimmunity Research Laboratory lead by Dr Michael W Jackson at the Department of Immunology at Flinders University, South Australia.
I am incredibly excited to kick-start the collaboration by visiting their lab in mid-March. We hope that this will lead to new insights about the origin of the ZnT8 autoantibodies and their possible role in the ongoing autoimmune response. The findings could enable prevention via immune tolerance in individuals at high risk for developing type 1 diabetes. Also, it may aid in designing immune therapies and enrol subjects in intervention trials.
Moving forward, I hope to increase the opportunity to work in an interdisciplinary environment with patients, physicians and nurses, industry, entrepreneurs, and designers. I would also like to establish a long-term collaboration between two world leading institutes of type 1 diabetes and autoimmunity, resulting in a wider network for further collaboration projects.