Regulatory T cells (Tregs) prevent excessive immune reactions in healthy people. In the development of autoimmune type 1 diabetes, this protection is not sufficiently effective. Researchers at Helmholtz Zentrum München and LMU Munich have now deciphered a mechanism that impairs Treg differentiation and stability.
In the study, when researchers inhibited the molecule that triggers this mechanism, an increased number of functional Tregs were formed again and autoimmune activation was reduced. This may represent a new molecular target to delay or even prevent the development of type 1 diabetes. The study was carried out within the framework of the German Center for Diabetes Research (DZD), and the results have now been published in Nature Communications.
Type 1 diabetes is the most common metabolic disease in children and adolescents. In this autoimmune disease, the body’s own immune cells gradually destroy the insulin-producing beta cells in the pancreas. Normally, Tregs prevent an attack on the body’s own cells. However, during the development of type 1 diabetes, this protection is insufficient. The team led by Professor Carolin Daniel is investigating why this is the case. She is research group leader at the Institute of Diabetes Research (IDF) at Helmholtz Zentrum München, scientist in the DZD and professor for immune modulation at Ludwig- Maximilians-Universität in Munich. The researchers have now deciphered a molecular mechanism that, during an early phase of type 1 diabetes, leads to the formation of decreased numbers of functional Tregs.
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