In a study recently published in the journal Endocrinology, Dr. Thomas Burris of St. Louis University reported a new method to prevent type 1 diabetes in a mouse model. Type 1 diabetes is a chronic autoimmune disease. The unique immune system destroys insulin-producing beta cells and prevents them from secreting insulin normally, leading to insulin deficiency and hyperglycemia. At present, the main method of treating type 1 diabetes is to control blood sugar levels through insulin therapy, which usually endangers the lives of patients. Burris and his research team focused on blocking the autoimmune process that destroys β cells, with the goal of developing treatments that prevent the development of the disease, not after the onset of the disease. I'm. "In our experiment, no mice received treatment after severely destroying beta cells. This treatment delayed the onset of type 1 diabetes and even reduced insulin production. I believe it can be done. Treatment is needed."
Scientists already know that at least two types of T lymphocytes are involved in the occurrence of type 1 diabetes, but the role of another type of helper T cells (Thelpercell17, Th17) is currently unknown. In this study, the researchers found that two nuclear receptors (nuclear receptors) play an important role in the development of Th17, ROR-α and ROR-γt. They used Burris to invent the selective inverse agonist SR1001, targeting these two receptors, blocking autoimmunity in the mouse model and protecting beta cells. These results confirm that Th17 cells may play an important role in the development of type 1 diabetes, and the use of drugs targeting this cell type may be a new strategy for the treatment of diabetes.