1型糖尿病,动物实验 z-bo 2020-12-14 347

　　Recently, in a study published in the journal Endocrinology, Dr. Thomas Burris of St. Louis University reported a new method of preventing type 1 diabetes in a mouse model.

　　 Type 1 diabetes is a chronic autoimmune disease. The own immune system damages the beta cells that produce insulin, making them unable to secrete insulin normally, leading to insulin deficiency and high blood sugar. At present, the main method of treating type 1 diabetes is to control blood glucose levels through insulin therapy, and this treatment often accompanies the patient's life.

　　 Burris and his research team focused on blocking the autoimmune process that damages β cells, with the goal of developing therapies to prevent the occurrence of diseases, rather than treatments after the onset. He said: "In our experiment, none of the mice developed diabetes, even if we treated the beta cells after significant damage. We believe that this treatment will slow down the development of type 1 diabetes and may even relieve insulin. The necessity of therapy."

　　 Scientists already know that at least two types of T lymphocytes are involved in the development of type 1 diabetes. However, the role of another type of T helper cell (T helper cell 17, 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, namely ROR-α and ROR-γt. They used Burris to invent a selective inverse agonist SR1001 to target these two receptors, successfully blocking the autoimmunity of the mouse model and protecting β cells.

　　These results confirm that Th17 cells may play an important role in the development of type 1 diabetes, and also indicate that the use of drugs to target this cell type may become a new strategy for diabetes treatment.