Studies show that diabetes and the immune system ability to properly respond diabetics at greater risk for infections. High blood glucose levels negatively effect blood vessels, circulation, and the healing of wounds and have been found to be a significant cause of bacterial and fungal infections. The specifics of this heightened susceptibility are still being investigated with in vitro analysis of diabetes immune cells showing similarities to other autoimmune diseases.
Type 1 Diabetes and Immune System
In type 1 diabetes cells from the immune system target and destroy insulin-producing beta cells in the pancreas ultimately leading to a total lack of insulin. Scientist continue to study the cause for autoimmune diseases, with research consistently pointing to genetics and to a lesser extent environment. Research has also linked type 1 diabetes to other autoimmune disorders like anemia, thyroid disease, and Addison’s disease. In a Northwestern University study diabetes patients underwent a form of chemotherapy to destroy islet-killing immune cells followed by an injection of their own purified stem cells. Thirteen of fifteen patients were able to stop insulin therapy for a period of nine months to three years. The exact function is still unknown though its hypothesized that the immune system reboots to create only healthy cells.
Type 2 Diabetes and Immune System
A 2011 study by researchers at Stanford University Medical School and the University of Toronto seems to have uncovered an autoimmune connection in type 2 diabetes. Macrophages and immune T and B cells cause inflammation in the fatty tissue that surrounds the organs of the body. This process was observed in laboratory mice fed on a high-fat, high-calorie diet causing fat cells to surpass their blood supply and die resulting in an immune response (including T and B cells) to clean up the dead cells, preventing healthy fat cells from responding to insulin. The researchers then eliminated the immune response in the same mice, resulting in obesity and high glucose levels after several weeks. In a subsequent study the researcher closely examined B cells. Genetically engineering mice to lack B cells, the researchers found that the mice were protected from insulin resistance even when they became obese eating a high-fat, high-calorie diet. When the mice were then injected with B cells their fasting blood glucose was found to rise significantly. Moving the study into humans, test subjects were found to make a distinct set of antibodies for their own cell proteins, suggesting that these antibodies are part of the creation of insulin resistance. The possible diabetic uses of an antibody called anti-CD20 that targets and eliminates mature immune B cells is currently are being researched.
