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BACH2 regulates CD8+ T cell differentiation by controlling access of AP-1 factors to enhancers

ABSTRACT: T cell antigen receptor (TCR) signaling drives distinct responses depending upon the differentiation state and context of CD8+ T cells. We hypothesized that access of signal-dependent transcription factors (TFs) to enhancers is dynamically regulated to shape transcriptional responses to TCR signaling. We found that the TF BACH2 restrains terminal differentiation to enable generation of long-lived memory cells and protective immunity following viral infection. BACH2 was recruited to enhancers where it limited expression of TCR-driven genes by attenuating the availability of activator protein 1 (AP-1) sites to Jun family signal-dependent TFs. In naïve cells, this prevented TCR-driven induction of genes associated with terminal differentiation. Upon effector differentiation, reduced expression of BACH2 and its phosphorylation enabled unrestrained induction of TCR-driven effector programs.

ORGANISM(S): Mus musculus

PROVIDER: GSE77857 | GEO | 2016/05/09

SECONDARY ACCESSION(S): PRJNA311746

REPOSITORIES: GEO

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Transcription factor Bach2 attenuates T cell receptor induced transcription to control regulatory T cell differentiation and homeostasis [ChIP-seq]

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