Type 1 Diabetes Prevented in Mice
A team of scientists say they have developed a way to stop the process that results in type 1 diabetes. The study, which was conducted using a mouse model, also helped clarify the role of a certain type of T cell in type 1 diabetes.
This new study is the latest of several that have been published in recent years concerning attempts to stop the development of the autoimmune disease type 1 diabetes. The team consisted of experts from Scripps Research Institute in Florida and St. Louis University School of Medicine (SLUSM).
The team, under direction of Thomas P. Burris, of the Department of Pharmacological and Physiological Science, STUSM, focused on blocking two receptors (ROR alpha and gamma t) that play a critical part in the development of T-cells known as TH17. Previously, experts have not been certain about how TH17 cells were involved in type 1 diabetes.
Now, however, the scientists have learned that when they targeted these two receptors in mouse models, they were able to put a stop to the destruction of beta cells, which are responsible for producing insulin. In fact, when they blocked the receptors with SR1001 (a special substance developed by Burris), none of the treated mice developed diabetes compared with more than 70 percent of the mice in the control group, who did not receive SR1001.
The results of this study indicate that TH17 cells have a role in the development of type 1 diabetes and that targeting these cells could lead to a new way to treat or prevent the disease. The authors concluded that their work “would enable us to gain a broader perspective of the roles of the RORs in type diabetes an enable the design of more focused therapeutics to treat type 1 diabetes.”
Other studies to stop type 1 diabetes
Some of the other research that has been done and is ongoing regarding ways to prevent or stop type 1 diabetes includes the following.
At Karolinska Institute in Sweden, a team conducted research involving macrophages and cytokines in type 1 diabetes. Since macrophages (a type of immune system cell) are known to sometimes destroy beta cells, they wanted to see if they could instruct the cells to protect beta cells instead.
The scientists discovered which immune cells (called cytokines) could “talk” to the macrophages and “tell” them to protect rather than damage the beta cells. According to Robert Harris, the lead researcher, “We managed to achieve this aim, defining a novel combination of cytokines that confer on macrophages the ability to protect mice from developing type 1 diabetes.”
At the Faculty of Health and Medical Sciences at the University of Copenhagen, experts discovered that very low doses of drugs called lysine deacetylase inhibitors, which are used to treat a form of cancer called lymphoma, reduced the development of type 1 diabetes by 38 to 45 percent in mice. These drugs also resulted in a 200 percent rise in insulin content in the pancreas, reduced inflammation, and helped protect beta cells from destruction.
A University of Alabama mouse study found that the blood pressure drug verapamil can stop the manufacture of a specific protein that results in the death of beta cells in the pancreas. Researchers are hoping to test this idea in humans in the near future.
All of the studies discussed here, including the new one, involve mouse models. Therefore, much more research is necessary before we can hope to see whether any of these approaches to preventing type 1 diabetes will work in humans.
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Christensen DP et al. Lysine deacetylase inhibition prevents diabetes by chromatin-independent immunoregulation and B-cell protection. Proceedings of the National Academy of Sciences 2014 Jan 21; 111(3): 1055-59
Parsa R et al. Adoptive transfer of immunomodulatory M2 macrophages prevents type 1 diabetes in NOD mice. Diabetes 2012 Jun 28
Solt LA et al. ROR inverse agonist suppresses insulitis and prevents hyperglycemia in a mouse model of type 1 diabetes. Endocrinology 2015. DOI:10.1210/en.2014-1677