Cited by 187Cytokine Signaling Pathways and InteractionsNF-κB Signaling PathwaysT-cell and B-cell Immunology

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Cutting Edge: A Transcriptional Repressor and Corepressor Induced by the STAT3-Regulated Anti-Inflammatory Signaling Pathway

El Kasmi, Karim C, Smith, Amber M, Williams, Lynn, Neale, Geoffrey, Panopolous, Athanasia, Watowich, Stephanie S, Häcker, Hans, Foxwell, Brian M J, Murray, Peter J·2007·The Journal of Immunology

DOI 10.4049/jimmunol.179.11.7215

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Abstract

IL-10 regulates anti-inflammatory signaling via the activation of STAT3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on proinflammatory mediator production. In this study we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3, and a helicase family corepressor, Strawberry notch homologue 2 (SBNO2), in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway regulated by IL-10 but not by STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 repressed NF-kappaB- but not IFN regulatory factor 7 (IRF7)-activated transcriptional reporters. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10.

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Authors: El Kasmi, K. C., Smith, A. M., Williams, L., Neale, G., Panopolous, A., Watowich, S. S., Häcker, H., Foxwell, B. M. J., & Murray, P. J.
Affiliations: Department of Infectious Diseases, St. Jude Children’s Research Hospital , Memphis, TN 38105
St. Jude Children's Research Hospital (US)
Imperial College London (GB)
The University of Texas MD Anderson Cancer Center (US)
ORCID: Smith, Amber M
Williams, Lynn
Neale, Geoffrey
Watowich, Stephanie S
Murray, Peter J
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2007-12-01
Volume: 179
Issue: 11
Pages: 7215-7219
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.179.11.7215
OpenAlex: W2127303484
Cited by: 182
References: 30
Citations by year: 2026: 5 · 2025: 10 · 2024: 13 · 2023: 15 · 2022: 9 · 2021: 15 · 2020: 8 · 2019: 8 · 2018: 8 · 2017: 5 · 2016: 8 · 2015: 10 · 2014: 6 · 2013: 11 · 2012: 14
FWCI: 4.89
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (T32CA009598, P 30CA 21765, P30CA021765, T32 CA09598-16)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: IL-10, STAT3 signaling, transcriptional repressor, corepressors, anti-inflammatory signaling, macrophages, NF-κB, IRF7, interleukin-6
MeSH terms: Animals, Anti-Inflammatory Agents, Non-Steroidal, Cell Line, Gene Expression Regulation, Humans, Macrophages, Mice, Inbred C57BL, Repressor Proteins, RNA, Messenger, Time Factors, Transcription Factors, Signal Transduction, Interleukin-10, Mice, Knockout, RNA, Small Interfering, Proto-Oncogene Proteins c-ets, STAT3 Transcription Factor, Mice

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Cutting Edge: A Transcriptional Repressor and Corepressor Induced by the STAT3-Regulated Anti-Inflammatory Signaling Pathway

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