ENAGenomicsImmunology, Department of Immunology, Graduate School of Medicine, Ehime Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA272912Mus musculusxref:PubMed:27581382It is becoming clear that the acquisition of T cell functions is closely linked to the reprogramming of the metabolic pathway. However, the impact of metabolic changes on the differentiation of helper T cell subsets remains unclear. We herein demonstrate a critical role of glutamine metabolism in regulating type 2-immune response. Bach2, a transcriptional repressor, binds to an AP-1 motif, and suppresses Th2 cell differentiation and glutaminolysis. Glutaminase 2, which controls glutamine metabolism, was identified as a Bach2 target gene. The pharmacological inhibition of glutamine metabolism normalized allergic lung inflammation that developed spontaneously in T-cell specific Bach2-deficient mice. These findings reveal the importance of the Bach2-dependent modulation of glutamine metabolism in regulating Th2 cell differentiation and Th2 cell- mediated inflammation. Overall design: Gene expression in Bach2 WT-Th (Bach2 WT-Th (-)), Bach2 KO-Th (Bach2 KO-Th (-)), restimulated Bach2 WT-Th (Bach2 WT Th (+)) and re-stimulated Bach2 KO-Th (Bach2 KO Th (+)).ENAfalseMus musculusBach2 inhibits Th2-type immune responses by regulating glutamine metabolism [expression array]2025-09-242024-04-04PRJNA272912GSE650831009027581382