TonEBP suppresses IL-10-mediated immunomodulation.

Citation data:

Scientific reports, ISSN: 2045-2322, Vol: 6, Issue: 1, Page: 25726

Publication Year:
2016
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Repository URL:
http://scholarworks.unist.ac.kr/handle/201301/19217
PMID:
27160066
DOI:
10.1038/srep25726
PMCID:
PMC4861964
Author(s):
Choi, Soo Youn, Lee, Hwan Hee, Lee, Jun Ho, Ye, Byeong Jin, Yoo, Eun Jin, Kang, Hyun Je, Jung, Gyu Won, An, Seung Min, Lee-Kwon, Whaseon, Chiong, Mario, Lavandero, Sergio, Kwon, Hyug Moo Show More Hide
Publisher(s):
Springer Nature, NATURE PUBLISHING GROUP
Tags:
Multidisciplinary, TONICITY-RESPONSIVE ENHANCER, TRANSCRIPTION FACTOR NFAT5, MACROPHAGE ACTIVATION, NUCLEAR-FACTOR, INSULIN-RESISTANCE, IL-10, CELLS, GENE, INTERLEUKIN-10, POLARIZATION
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article description
TonEBP is a key transcriptional activator of M1 phenotype in macrophage, and its high expression is associated with many inflammatory diseases. During the progression of the inflammatory responses, the M1 to M2 phenotypic switch enables the dual role of macrophages in controlling the initiation and resolution of inflammation. Here we report that in human and mouse M1 macrophages TonEBP suppresses IL-10 expression and M2 phenotype. TonEBP knockdown promoted the transcription of the IL-10 gene by enhancing chromatin accessibility and Sp1 recruitment to its promoter. The enhanced expression of M2 genes by TonEBP knockdown was abrogated by antagonism of IL-10 by either neutralizing antibodies or siRNA-mediated silencing. In addition, pharmacological suppression of TonEBP leads to similar upregulation of IL-10 and M2 genes. Thus, TonEBP suppresses M2 phenotype via downregulation of the IL-10 in M1 macrophages.

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