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Involvement of NF-kB in TGF-β-mediated suppression of IL-4 signaling.

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/28118

Title: Involvement of NF-kB in TGF-β-mediated suppression of IL-4 signaling.
Authors: Yamamoto, Tetsuya Browse this author
Imoto, Seiyu Browse this author
Sekine, Yuichi Browse this author
Sugiyama, Kenji Browse this author
Akimoto, Toshihiko Browse this author
Muraguchi, Atsushi Browse this author
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: IL-4
TGF-β
STAT6
NF-κB
Issue Date: 16-Jan-2004
Publisher: Elsevier
Journal Title: Biochemical and Biophysical Research Communications
Volume: 313
Issue: 3
Start Page: 627
End Page: 634
Publisher DOI: 10.1016/j.bbrc.2003.11.163
PMID: 14697238
Abstract: Control of immune response requires the coordinated integration of both stimulatory and inhibitory factors. Therefore, the cross-talk of different signaling pathways is critical in providing an integrated cellular response to multiple external signals. Both interleukin-4 (IL-4) and transforming growth factor (TGF-β) are pleiotropic cytokines and play critical roles in controlling immune responses. For example, IL-4 mediates important pro-inflammatory functions in asthma including induction of the IgE isotype switch and expression of vascular cell adhesion molecules. Whereas, TGF-β is secreted from B, T, and dendritic cells as well as macrophages, and negatively regulates their proliferation, differentiation, and activation by other cytokines. In this study, we examined the effect of TGF-β on IL-4 signaling using B cells as well as embryonic kidney cells. TGF-β inhibited IL-4-induced IgG1 production and gene expression of germline ε transcripts in B cells. In embryonic kidney cells, TGF-β signals suppressed IL-4-induced transcription, when we monitored using germline ε promoter DNA. Furthermore, activation of NF-κB resulted in a resistance to TGF-β-mediated suppression of IL-4 signaling. These results indicate that TGF-β-mediated regulation of IL-4 signaling may act by targeting NF-κB signaling.
Relation: http://www.sciencedirect.com/science/journal/0006291X
Type: article (author version)
URI: http://hdl.handle.net/2115/28118
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

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