Abstract
Immunoglobulin E (IgE) production is induced by interleukin (IL)-4 signaling mediated by type I IL-4 receptor (IL-4R) in B cells. We found that flavones inhibited IL-4-induced epsilon germline transcription which is essential for IgE class switching, and the phosphorylation of signal transducer and activator of transcription 6, janus kinase 3, and IL-4Ralpha, whereas IL-4 signaling mediated through type II IL-4R was unaffected by flavones. Furthermore, flavones reduced the expression of common gamma chain, a characteristic constituent subunit of type I IL-4R, suggesting that flavones suppress type I IL-4R signaling.
Copyright 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
MeSH terms
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Apigenin / pharmacology
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Blotting, Western
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Cell Line, Tumor
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Down-Regulation / drug effects
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Flavones / pharmacology*
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Flavonoids / pharmacology
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Gene Expression / drug effects
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HeLa Cells
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Humans
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Immunoglobulin epsilon-Chains / genetics
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Immunoglobulin epsilon-Chains / metabolism
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Interleukin Receptor Common gamma Subunit / genetics
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Interleukin Receptor Common gamma Subunit / metabolism*
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Interleukin-4 / pharmacology
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Interleukin-4 Receptor alpha Subunit / metabolism
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Janus Kinase 3 / metabolism
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PPAR gamma / genetics
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PPAR gamma / metabolism
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Phosphorylation / drug effects
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RNA Interference
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Receptors, Interleukin-4, Type I / genetics
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Receptors, Interleukin-4, Type I / metabolism*
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Reverse Transcriptase Polymerase Chain Reaction
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STAT6 Transcription Factor / metabolism
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Signal Transduction / drug effects*
Substances
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Flavones
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Flavonoids
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Immunoglobulin epsilon-Chains
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Interleukin Receptor Common gamma Subunit
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Interleukin-4 Receptor alpha Subunit
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PPAR gamma
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Receptors, Interleukin-4, Type I
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STAT6 Transcription Factor
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Interleukin-4
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chrysin
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Apigenin
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Janus Kinase 3