Throwing a spanner in the workings of diabetes
Type-1 Diabetes mellitus (T1D) develops when autoreactive T lymphocytes destroy insulin-producing tissues, which leads to a shortage of insulin. The 'Role of the alpha4 integrin (CD49d) in type-1 diabetes mellitus prevention and treatment' (CD49D IN DIABETES) project aims to discover a means of protecting or even regenerating the islet cell mass when T1D diagnosis is first made. This would help reduce the severity of or cure T1D and bring down morbidity and mortality rates. To test this hypothesis, researchers are working with CD49d, which is a dominant homing receptor for inflammatory lymphocytes. This is a surface protein involved in cellular binding and the process of cell adhesion. Project partners believe that blocking alpha-4 integrin adhesion in the pre-diabetic state or during early diabetes can halt ongoing movement of autoreactive T-cells to inflamed pancreatic tissue. This approach has already been shown to have therapeutic results in various inflammatory conditions, including autoimmune diseases. CD49D IN DIABETES suggests this action could protect the remaining insulin-producing cells and might even act to prevent or delay T1D if performed during pre-diabetes (secondary prevention). This hypothesis is being tested in a new genetic mouse model using a non-obese diabetic (NOD) strain. The aim is to test the potential as a treatment for newly diagnosed T1D patients. Three mouse strains have been bred up to eighth and even ninth generation. Researchers test regularly for the proneness of NOD breeders to diabetes, and expect that on reaching the 10th generation they will have 'pure' NOD mice. These can then be used as founders for the planned studies scheduled to begin in the second or third quarter of 2011.
