Abstract
Regulatory T cells (Tregs) are critical for peripheral immune tolerance and homeostasis, and altered Treg behavior is involved in many pathologies, including autoimmunity and cancer. The expression of the transcription factor FoxP3 in Tregs is fundamental to maintaining their stability and immunosuppressive function. Recent studies have highlighted the crucial role that metabolic reprogramming plays in controlling Treg plasticity, stability, and function. In this review, we summarize how the availability and use of various nutrients and metabolites influence Treg metabolic pathways and activity. We also discuss how Treg‐intrinsic metabolic programs define and shape their differentiation, FoxP3 expression, and suppressive capacity. Lastly, we explore how manipulating the regulation of Treg metabolism might be exploited in different disease settings to achieve novel immunotherapies.
Highlights
Regulatory T cells (Tregs) are a subset of CD4+ T helper (Th) cells that is indispensable for the maintenance of peripheral tolerance and immune homeostasis [1,2]
Current studies of energy metabolism in Tregs indicate that Treg proliferation and suppressive activity can be influenced by a variety of metabolic pathways, including anabolic signals driven by the mTOR complex 1 (mTORC1) axis and those arising from FoxP3dependent oxidative metabolism [22,61]
The studies we have reviewed highlight the multifaceted relationships between the intrinsic and extrinsic metabolic pathways modulating Treg function, and their significant implications for the treatment of immune-related diseases
Summary
Regulatory T cell metabolism at the intersection between autoimmune diseases and cancer Kurniawan, Henry; Soriano-Baguet, Leticia; Brenner, Dirk. Regulatory T cell metabolism at the intersection between autoimmune diseases and cancer. Terms of use This work is brought to you by the University of Southern Denmark. Regulatory T cell metabolism at the intersection between autoimmune diseases and cancer Henry Kurniawan∗1,2, Leticia Soriano-Baguet∗1,2,3 and Dirk Brenner. The expression of the transcription factor FoxP3 in Tregs is fundamental to maintaining their stability and immunosuppressive function. Recent studies have highlighted the crucial role that metabolic reprogramming plays in controlling Treg plasticity, stability, and function. We summarize how the availability and use of various nutrients and metabolites influence Treg metabolic pathways and activity. We discuss how Treg-intrinsic metabolic programs define and shape their differentiation, FoxP3 expression, and suppressive capacity. We explore how manipulating the regulation of Treg metabolism might be exploited in different disease settings to achieve novel immunotherapies
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