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A previous study reported that -KG, the metabolite of Glu, is more abundant in Th17 cells than in Treg cells, suggesting that glutaminolysis may be more active in Th17 cells (47).Further mechanistic findings revealed that 2-hydroxyglutarate (2-HG), a direct product of error-prone dehydrogenase activity on -KG, could trigger hypermethylation of the Foxp3 gene and inhibit Foxp3 transcription, thereby inhibiting the differentiation of Treg cells and regulating Th17/Treg homeostasis through epigenetic mechanisms ( Figure 2 ) (48)

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