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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
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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