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

被引：203

作者：

Roychoudhuri, Rahul ^{[1
,2
]}

Clever, David ^{[1
,3
]}

Li, Peng ^{[4
,5
]}

Wakabayashi, Yoshiyuki ^{[6
]}

Quinn, Kylie M. ^{[7
]}

Klebanoff, Christopher A. ^{[1
]}

Ji, Yun ^{[1
]}

Sukumar, Madhusudhanan ^{[1
]}

Eil, Robert L. ^{[1
]}

Yu, Zhiya ^{[1
]}

Spolski, Rosanne ^{[4
,5
]}

Palmer, Douglas C. ^{[1
]}

Pan, Jenny H. ^{[1
]}

Patel, Shashank J. ^{[1
]}

Macallan, Derek C. ^{[8
]}

Fabozzi, Giulia ^{[1
]}

Shih, Han-Yu ^{[9
]}

Kanno, Yuka ^{[9
]}

Muto, Akihiko ^{[10
,11
]}

Zhu, Jun ^{[6
]}

Gattinoni, Luca ^{[1
]}

O'Shea, John J. ^{[9
]}

Okkenhaug, Klaus ^{[2
]}

Igarashi, Kazuhiko ^{[10
,11
]}

Leonard, Warren J. ^{[4
,5
]}

Restifo, Nicholas P. ^{[1
,12
]}

机构：

[1] NCI, NIH, Bethesda, MD 20892 USA

[2] Babraham Inst, Lab Lymphocyte Signalling & Dev, Cambridge, England

[3] Ohio State Univ, Coll Med, Med Scientist Training Program, Columbus, OH 43210 USA

[4] NHLBI, Lab Mol Immunol, NIH, Bldg 10, Bethesda, MD 20892 USA

[5] NHLBI, Ctr Immunol, NIH, Bldg 10, Bethesda, MD 20892 USA

[6] NHLBI, Syst Biol Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA

[7] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD USA

[8] St Georges Univ London, Inst Infect & Immun, London, England

[9] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA

[10] Tohoku Univ, Dept Biochem, Grad Sch Med, Sendai, Miyagi 980, Japan

[11] Japan Agcy Med Res & Dev, AMED CREST, Tokyo, Japan

[12] Georgetown Univ, Med Ctr, Grad Program Microbiol & Immunol, Washington, DC 20007 USA

来源：

NATURE IMMUNOLOGY | 2016年 / 17卷 / 07期

基金：

英国惠康基金; 英国生物技术与生命科学研究理事会;

关键词：

TRANSCRIPTION FACTORS; EXPRESSION ANALYSIS; MEMORY PHENOTYPE; EFFECTOR; GENE; REPRESSES; LYMPHOCYTES; ACTIVATION; GENERATION; PROTEINS;

D O I：

10.1038/ni.3441

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：851 / +

页数：12

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