It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
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.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Department of Dermatology, Venerology and Allergology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
2 Department of Dermatology, Venerology and Allergology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany; Institute for Transfusion Medicine and Immunology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
3 Institute for Transfusion Medicine and Immunology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
4 Center for Medical Research, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
5 Institute of Molecular Immunology, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Munich, Germany
6 Department of Pathology and Laboratory Medicine, University of Groningen, University of Groningen Medical Center, Groningen, The Netherlands
7 Department of Dermatology, Venerology and Allergology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany; Institute of Carcinogeneis, NN Blokhin Russian Cancer Research Center, Moscow, Russia
8 Department of Dermatology, Venerology and Allergology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany; Institute for Transfusion Medicine and Immunology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany; Red Cross Blood Service Baden-Württemberg–Hessen, Mannheim, Germany