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Interaction of Ets-1 with HDAC1 represses IL-10 expression in Th1 cells

Title
Interaction of Ets-1 with HDAC1 represses IL-10 expression in Th1 cells
Authors
Lee C.-G.Kwon H.-K.Sahoo A.Hwang W.So J.-S.Hwang J.-S.Chae C.-S.Kim G.-C.Kim J.-E.So H.-S.Hwang E.S.Grenningloh R.Ho I.-C.Im S.-H.
Ewha Authors
황은숙
SCOPUS Author ID
황은숙scopus
Issue Date
2012
Journal Title
Journal of Immunology
ISSN
0022-1767JCR Link
Citation
vol. 188, no. 5, pp. 2244 - 2253
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
IL-10 is a multifunctional cytokine that plays a crucial role in immunity and tolerance. IL-10 is produced by diverse immune cell types, including B cells and subsets of T cells. Although Th1 produce IL-10, their expression levels are much lower than Th2 cells under conventional stimulation conditions. The potential role of E26 transformation-specific 1 (Ets-1) transcription factor as a negative regulator for Il10 gene expression in CD4 + T cells has been implicated previously. In this study, we investigated the underlying mechanism of Ets-1-mediated Il10 gene repression in Th1 cells. Compared with wild type Th1 cells, Ets-1 knockout Th1 cells expressed a significantly higher level of IL-10, which is comparable with that of wild type Th2 cells. Upregulation of IL-10 expression in Ets-1 knockout Th1 cells was accompanied by enhanced chromatin accessibility and increased recruitment of histone H3 acetylation at the Il10 regulatory regions. Reciprocally, Ets-1 deficiency significantly decreased histone deacetylase 1 (HDAC1) enrichment at the Il10 regulatory regions. Treatment with trichostatin A, an inhibitor of HDAC family, significantly increased Il10 gene expression by increasing histone H3 acetylation recruitment. We further demonstrated a physical interaction between Ets-1 and HDAC1. Coexpression of Ets-1 with HDAC1 synergistically repressed IL-10 transcription activity. In summary, our data suggest that an interaction of Ets-1 with HDAC1 represses the Il10 gene expression in Th1 cells. Copyright © 2012 by The American Association of Immunologists, Inc.
DOI
10.4049/jimmunol.1101614
Appears in Collections:
약학대학 > 약학과 > Journal papers
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