TonEBP suppresses IL-10-mediated immunomodulation

Soo Youn Choi; Hwan Hee Lee; Jun Ho Lee; Byeong Jin Ye; Eun Jin Yoo; Hyun Je Kang; Gyu Won Jung; Seung Min An; Whaseon Lee-Kwon; Mario Chiong; Sergio Lavandero; Hyug Moo Kwon

doi:10.1038/srep25726

TonEBP suppresses IL-10-mediated immunomodulation

Soo Youn Choi, Hwan Hee Lee, Jun Ho Lee, Byeong Jin Ye, Eun Jin Yoo, Hyun Je Kang, Gyu Won Jung, Seung Min An, Whaseon Lee-Kwon, Mario Chiong, Sergio Lavandero, Hyug Moo Kwon

Universidad de Chile

Research output: Contribution to journal › Article › peer-review

24 Citations (Scopus)

Abstract

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.

Original language	English
Article number	25726
Journal	Scientific Reports
Volume	6
DOIs	https://doi.org/10.1038/srep25726
Publication status	Published - May 10 2016

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title = "TonEBP suppresses IL-10-mediated immunomodulation",

abstract = "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.",

author = "Choi, {Soo Youn} and Lee, {Hwan Hee} and Lee, {Jun Ho} and Ye, {Byeong Jin} and Yoo, {Eun Jin} and Kang, {Hyun Je} and Jung, {Gyu Won} and An, {Seung Min} and Whaseon Lee-Kwon and Mario Chiong and Sergio Lavandero and Kwon, {Hyug Moo}",

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AU - Choi, Soo Youn

AU - Lee, Hwan Hee

AU - Lee, Jun Ho

AU - Ye, Byeong Jin

AU - Yoo, Eun Jin

AU - Kang, Hyun Je

AU - Jung, Gyu Won

AU - An, Seung Min

AU - Lee-Kwon, Whaseon

AU - Chiong, Mario

AU - Lavandero, Sergio

AU - Kwon, Hyug Moo

PY - 2016/5/10

Y1 - 2016/5/10

N2 - 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.

AB - 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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TonEBP suppresses IL-10-mediated immunomodulation

Abstract

ASJC Scopus Subject Areas

UN SDGs

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