Fighting Metabolic Diseases Through Immune Modulation
A study led by researchers from Helmholtz Munich and the German Center for Diabetes Research (DZD) unveils a key communication pathway between the immune system and metabolism in the hypothalamic region of the brain. By identifying the role of regulatory T-cells (Tregs) in metabolic regulation, the team opens new avenues for immune-targeted treatments of metabolic diseases like obesity and type 2 diabetes.
The global rise in obesity is associated with many health risks, including chronic low-grade inflammation triggered by high caloric diets. But how do the immune system and metabolism interact?
Researchers from Helmholtz Munich and the German Center for Diabetes Research (DZD) pinpointed a key player in this connection: regulatory T-cells (Tregs) in the hypothalamus. Their findings reveal that beyond their well-known role in immune regulation, these cells also support metabolic balance. In mice, an enrichment of Tregs in hypothalamic tissue was essential for limiting immune activation of microglial cells and infiltrating macrophages in response to hypercaloric diet.
Published in Nature Communications, this discovery contributes to a paradigm shift in the fields of metabolism and immunology. While the recruitment of T cells to the brain was thought to be pathogenic, the role of Tregs in the hypothalamus can be beneficial, underscoring their potential for the treatment of diseases like obesity as well as type 2 diabetes and metabolic disease.
“For the first time, we demonstrate that protective Treg cells regulate immune activation in the hypothalamus and counteract metabolic impairments caused by high-calorie intake,” says lead author Carolin Daniel. “Our findings may contribute to the development of Treg-centered precision immune modulation for metabolic disease.”
Original Publication
Becker et al., 2025: Regulatory T cells in the mouse hypothalamus control immune activation and ameliorate metabolic impairments in high-calorie environments. Nature Communications. DOI: https://doi.org/10.1038/s41467-025-57918-z
