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Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4+ T cells
Eunkyeong Jang1, Hye Rim Lee1, Geon Hee Lee1, Ah-Reum Oh2, Ji-Young Cha2, Kazuhiko Igarashi3, Jeehee Youn1,*
1Department of Anatomy and Cell Biology, Hanyang University,
2Department of Biochemistry, Gachon University,
3Department of Biochemistry, Tohoku University Graduate School of Medicine
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.
Abstract, Accepted Manuscript(in press) [Submitted on July 10, 2017, Accepted on August 28, 2017]
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