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

Roychoudhuri, Rahul; Clever, David; Li, Peng; Wakabayashi, Yoshiyuki; Quinn, Kylie M; Klebanoff, Christopher A; Ji, Yun; Sukumar, Madhusudhanan; Eil, Robert L; Yu, Zhiya; Spolski, Rosanne; Palmer, Douglas C; Pan, Jenny H; Patel, Shashank J; Macallan, Derek C; Fabozzi, Giulia; Shih, Han-Yu; Kanno, Yuka; Muto, Akihiko; Zhu, Jun; Gattinoni, Luca; O'Shea, John J; Okkenhaug, Klaus; Igarashi, Kazuhiko; Leonard, Warren J; Restifo, Nicholas P.
Nat Immunol; 17(7): 851-860, 2016 07.
Artigo em Inglês | MEDLINE | ID: mdl-27158840
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.
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