ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/005/SRR1654785/SRR1654785.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/004/SRR1654784/SRR1654784.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/003/SRR1654783/SRR1654783.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/006/SRR1654786/SRR1654786.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/001/SRR1654781/SRR1654781.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR165/002/SRR1654782/SRR1654782.fastq.gzprimary200OKGenomicsImmunology, Department of Immunology, Graduate School of Medicine, Ehime Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA267601Mus 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: Examination of transcriptional factor Bach2 binding and histone modefications in Bach2 WT and KO CD4 T cellsENAfalseMus musculusBach2 inhibits Th2-type immune responses by regulating glutamine metabolism [ChIP-seq]2025-09-242023-03-28PRJNA267601GSE633801009027581382