Abstract
In this issue of Cell Metabolism, Hochrein etal. identify a metabolic checkpoint controlling the transcriptional programming of effector CD4+ Tcells. The authors show that GLUT3-mediated glucose import and ACLY-dependent acetyl-CoA generation control histone acetylation and, hence, the epigenetic imprinting of effector gene expression in differentiated effector CD4+ Tcells. These findings suggest a novel therapeutic target for inflammation-associated diseases.
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