Bach2 represses the AP-1-driven induction of interleukin-2 gene transcription in CD4(+) T cellsopen access
- Authors
- Jang, Eunkyeong; Lee, Hye Rim; Lee, Geon Hee; Oh, Ah-Reum; Cha, Ji-Young; Igarashi, Kazuhiko; Youn, Jeehee
- Issue Date
- Sep-2017
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
- Keywords
- Bach2; CD4(+) T cells; IL-2; Repressor
- Citation
- BMB REPORTS, v.50, no.9, pp.472 - 477
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- BMB REPORTS
- Volume
- 50
- Number
- 9
- Start Page
- 472
- End Page
- 477
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/151720
- DOI
- 10.5483/BMBRep.2017.50.9.124
- ISSN
- 1976-6696
- 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.
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