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IL-4 driven transcription factor FoxQ1 is expressed by monocytes in atopic dermatitis and stimulates monocyte migration

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Published in: Scientific reports 7(2017) Artikel-Nummer 16847, 9 Seiten
Authors and Corporations: Ovsiy, Ilja (Author), Riabov, Vladimir (Author), Manousaridis, Ioannis (Author), Michel, Julia (Author), Moganti, Kondaiah (Author), Yin, Shuiping (Author), Liu, Tengfei (Author), Sticht, Carsten (Author), Goerdt, Sergij (Author), Gratchev, Alexei (Author), Kzhyshkowska, Julia (Author)
Other Authors: Riabov, Vladimir 1983- [Author] • Manousaridis, Ioannis 1983- [Author] • Michel, Julia [Author] • Moganti, Kondaiah 1985- [Author] • Yin, Shuiping 1987- [Author] • Liu, Tengfei 1987- [Author] • Sticht, Carsten 1972- [Author] • Goerdt, Sergij 1954- [Author] • Gratchev, Alexei 1972- [Author] • Kzhyshkowska, Julia 1967- [Author]
Type of Resource: E-Book Component Part
Language: English
published:
04 December 2017
Series: Scientific reports, 7(2017) Artikel-Nummer 16847, 9 Seiten
Source: Verbunddaten SWB
Lizenzfreie Online-Ressourcen
ISSN: 2045-2322
Description
Summary: Monocytes are actively recruited at sites of chronic inflammation. However, molecular factors involved in this process are not fully elucidated. Here, we show that cytokine IL-4 which is implicated in the development of chronic inflammatory disease atopic dermatitis (AD) induces expression of transcription factor FoxQ1 in human monocytes and macrophages. FoxQ1 mRNA levels were elevated in monocytes of AD patients compared to healthy donors. Overexpression of FoxQ1 in RAW 264.7 monocytic cells facilitated their migration towards MCP-1 and was associated with decreased expression of migration-regulating genes (claudin 11 and plexin C1). Furthermore, FoxQ1 overexpression in RAW cells accelerated TNFα secretion after LPS challenge. Overall, our results indicate that FoxQ1 stimulates monocyte motility, increases pro-inflammatory potential, and directs monocyte migration towards MCP-1 that is crucial for monocyte influx into inflammatory sites. This mechanism could contribute to the pathogenesis of chronic inflammatory disorders such as AD.
Item Description: Gesehen am 26.04.2018
Physical Description: 9
ISSN: 2045-2322
DOI: 10.1038/s41598-017-17307-z