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Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4+ T cells

  • Jang, Eunkyeong (Laboratory of Autoimmunology, Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Lee, Hye Rim (Laboratory of Autoimmunology, Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Lee, Geon Hee (Laboratory of Autoimmunology, Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Oh, Ah-Reum (Department of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, Gachon University) ;
  • Cha, Ji-Young (Department of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, Gachon University) ;
  • Igarashi, Kazuhiko (Department of Biochemistry, Tohoku University Graduate School of Medicine) ;
  • Youn, Jeehee (Laboratory of Autoimmunology, Department of Anatomy and Cell Biology, College of Medicine, Hanyang University)
  • Received : 2017.07.10
  • Accepted : 2017.08.28
  • Published : 2017.09.30

Abstract

The transcription repressor Bach2 has been proposed as a regulator of T cell quiescence, but the underlying mechanism is not fully understood. Given the importance of interleukin-2 in T cell activation, we investigated whether Bach2 is a component of the network of factors that regulates interleukin-2 expression. In primary and transformed $CD4^+$ T cells, Bach2 overexpression counteracted T cell receptor/CD28- or PMA/ionomycin-driven induction of interleukin-2 expression, and silencing of Bach2 had the opposite effect. Luciferase and chromatin immunoprecipitation assays revealed that Bach2 binds to multiple Maf-recognition element-like sites on the interleukin-2 proximal promoter in a manner competitive with AP-1, and thereby represses AP-1-driven induction of interleukin-2 transcription. Thus, this study demonstrates that Bach2 is a direct repressor of the interleukin-2 gene in $CD4^+$ T cells during the immediate early phase of AP-driven activation, thereby playing an important role in the maintenance of immune quiescence in the steady state.

Keywords

References

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