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Roles of CCAAT/enhancer-binding protein in transcriptional regulation of the human IL-5 gene

Abstract Interleukin-5 (IL-5) plays a critical role in the pathogenesis of eosinophil-associated allergic disorders, such as asthma. IL-5 may also play a major role in the development of eosinophilia-associated lymphoproliferative disorders caused by human T lymphotropic virus type?I (HTLV-I). In th...

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Hauptverfasser: Li-Weber, Min (VerfasserIn) , Giaisi, Marco (VerfasserIn) , Krammer, Peter H. (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 29 November 2001
In: European journal of immunology
Year: 2001, Jahrgang: 31, Heft: 12, Pages: 3694-3703
ISSN:1521-4141
DOI:10.1002/1521-4141(200112)31:12<3694::AID-IMMU3694>3.0.CO;2-S
Online-Zugang:Verlag, Volltext: https://doi.org/10.1002/1521-4141(200112)31:12<3694::AID-IMMU3694>3.0.CO;2-S
Verlag, Volltext: https://onlinelibrary.wiley.com/doi/full/10.1002/1521-4141(200112)31:12%3C3694::AID-IMMU3694%3E3.0.CO;2-S
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Verfasserangaben:Min Li-Weber, Marco Giaisi and Peter H. Krammer

MARC

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520 |a Abstract Interleukin-5 (IL-5) plays a critical role in the pathogenesis of eosinophil-associated allergic disorders, such as asthma. IL-5 may also play a major role in the development of eosinophilia-associated lymphoproliferative disorders caused by human T lymphotropic virus type?I (HTLV-I). In this study, we have investigated the control mechanisms for IL-5 production and found that ectopic expression of NF-IL6 (C/EBP?) increases endogenous IL-5 mRNA expression. The IL-5 promoter contains four C/EBP consensus sequences. We show here that one of the C/EBP site at ??235 promoter region binds to NF-IL6 protein with high affinity and interacts with NF-IL6 and NF-IL6? (C/EBPδ) in Jurkat T?cells. Mutations within the C/EBP sequence reduced the promoter activity in response to T?cell activation by more than 50?%. In addition, we show that in vivo inducible expression of Tax protein in Jurkat T?cells stably transfected with Tax further increased ionomycin plus phorbol ester stimulated IL-5 promoter activity. The effect of Tax on IL-5 promoter activity was abolished when the C/EBP site was mutated. Thus, the C/EBP site may be also involved in HTLV-I Tax-mediated up-regulation of IL-5 gene expression. Our data suggest that C/EBP proteins may regulate IL-5 gene expression in response to different stimulation signals. 
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