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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 on 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 after 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 naive 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.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Roychoudhuri R,Clever D,Li P,Wakabayashi Y,Quinn KM,Klebanoff CA,Ji Y,Sukumar M,Eil RL,Yu Z,Spolski R,Palmer DC,Pan JH,Patel SJ,Macallan DC,Fabozzi G,Shih HY,Kanno Y,Muto A,Zhu J,Gattinoni L,O'Shea JJ,Okkenhau

doi

10.1038/ni.3441

subject

Has Abstract

pub_date

2016-07-01 00:00:00

pages

851-860

issue

7

eissn

1529-2908

issn

1529-2916

journal_volume

17

pub_type

杂志文章

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