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http://dx.doi.org/10.5483/BMBRep.2017.50.9.124

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)
Publication Information
BMB Reports / v.50, no.9, 2017 , pp. 472-477 More about this Journal
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
Bach2; $CD4^+$ T cells; IL-2; Repressor;
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