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NF-κB synergizes with NF-AT and NF-IL6 in activation of the IL-4 gene in T cells

IL-4 plays a pivotal role in the development of the Th2 cell mediated humoral immune response and causes IgE-dependent allergic inflammatory diseases. Expression of IL-4 in differentiated Th2 cells is regulated by transcription factors such as NF-AT, AP-1 and NF-IL6. Recently, increasing evidence in...

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Bibliographic Details
Main Authors: Li-Weber, Min (Author) , Giaisi, Marco (Author) , Baumann, Sven (Author) , Pálfi, Katalin (Author) , Krammer, Peter H. (Author)
Format: Article (Journal)
Language:English
Published: 23 March 2004
In: European journal of immunology
Year: 2004, Volume: 34, Issue: 4, Pages: 1111-1118
ISSN:1521-4141
DOI:10.1002/eji.200324687
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1002/eji.200324687
Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/eji.200324687
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Author Notes:Min Li‐Weber, Marco Giaisi, Sven Baumann, Katalin Pálfi and Peter H. Krammer
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Summary:IL-4 plays a pivotal role in the development of the Th2 cell mediated humoral immune response and causes IgE-dependent allergic inflammatory diseases. Expression of IL-4 in differentiated Th2 cells is regulated by transcription factors such as NF-AT, AP-1 and NF-IL6. Recently, increasing evidence indicates that the pro-inflammatory transcription factor NF-κB may also participate inIL-4 expression. In this study, we show that the IL-4 promoter is synergistically activated by NF-κB, NF-AT and NF-IL6 at the NF-κB/NF-AT/NF-IL6 composite sites. In addition, we performed the chromatin immunoprecipitation technique to determine the functional relevance of NF-κB in the activation of the IL-4 gene in vivo. We demonstrate that NF-κB binds to the IL-4 promoter in vivo upon T cell activation. Inhibition of NF-κB nuclear translocation in living cells blocked binding of NF-κB to the IL-4 promoter. The data provide first evidence that NF-κB is directly involved in IL-4 transcription.
Item Description:Gesehen am 04.03.2021
Physical Description:Online Resource
ISSN:1521-4141
DOI:10.1002/eji.200324687

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