GSE63380
Bach2 inhibits Th2-type immune responses by regulating glutamine metabolism [ChIP-seq]
It 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 cells