『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=203504EID:203504, Map:0, LastModified:2013年7月19日(金) 18:37:18, Operator:[細川 義隆], Avail:TRUE, Censor:0, Owner:[細川 義隆], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
招待 (推奨):
審査 (推奨): Peer Review [継承]
カテゴリ (推奨): 研究 [継承]
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学究種別 (推奨):
組織 (推奨):
著者 (必須): 1.細川 義隆 ([徳島大学.病院.診療科.歯科.むし歯科(第一保存科)])
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2.細川 育子 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.歯科保存学])
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3.尾崎 和美 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.口腔保健学系.口腔保健支援学]/[徳島大学.歯学部.口腔保健学科.口腔保健支援学講座])
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4.中江 英明
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5.松尾 敬志
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題名 (必須): (英) TNFSF14 coordinately enhances CXCL10 and CXCL11 production from IFN-gamma-stimulated human gingival fibroblasts  (日)    [継承]
副題 (任意):
要約 (任意): (英) TNFSF14 is involved in the pathogenesis of some inflammatory diseases such as arthritis. CXCL10 and CXCL11 recruit Th1 cells, and the productions of these chemokines are related to the exacerbation of some inflammatory diseases including arthritis and periodontal disease. We examined in vitro effects of TNFSF14 on IFN-gamma-induced CXCL10 and CXCL11 production in human gingival fibroblasts (HGFs). HGFs constitutively expressed TNFSF14 receptors, LTbetaR and HVEM. TNFSF14 enhanced IFN-gamma-induced secretion of CXCL10 and CXCL11 from HGFs. IFN-gamma treatment increased HVEM expression on HGFs. TNFSF14 in combination with IFN-gamma resulted in increased activation of p38 MAPK, ERK and IkappaB-alpha compared with TNFSF14 or IFN-gamma alone. Moreover, inhibitors of p38 MAPK, ERK and NF-kappaB abolished the CXCL10 and CXCL11 productions from TNFSF14 with IFN-gamma-stimulated HGFs. These effects of TNFSF14 may promote the infiltration of Th1 cells into lesions with inflammatory diseases. TNFSF14 might act as a proinflammatory cytokine in some inflammatory diseases thus is a candidate therapeutic target.  (日)    [継承]
キーワード (推奨): 1. (英) Chemokine CXCL10 (日) (読) [継承]
2. (英) Chemokine CXCL11 (日) (読) [継承]
3. (英) Extracellular Signal-Regulated MAP Kinases (日) (読) [継承]
4. (英) Fibroblasts (日) (読) [継承]
5. (英) Gingiva (日) (読) [継承]
6. (英) Humans (日) (読) [継承]
7. (英) I-kappa B Proteins (日) (読) [継承]
8. (英) Interferon-gamma (日) (読) [継承]
9. (英) Lymphotoxin beta Receptor (日) (読) [継承]
10. (英) MAP Kinase Kinase Kinases (日) (読) [継承]
11. (英) Phosphorylation (日) (読) [継承]
12. (英) Protein Kinase Inhibitors (日) (読) [継承]
13. (英) Proto-Oncogene Proteins (日) (読) [継承]
14. (英) RNA, Messenger (日) (読) [継承]
15. (英) Receptors, Tumor Necrosis Factor, Member 14 (日) (読) [継承]
16. (英) Signal Transduction (日) (読) [継承]
17. (英) Tumor Necrosis Factor Ligand Superfamily Member 14 (日) (読) [継承]
18. (英) Up-Regulation (日) (読) [継承]
発行所 (推奨): Elsevier Science [継承]
誌名 (必須): Molecular Immunology ([Elsevier Science])
(pISSN: 0161-5890, eISSN: 1872-9142)

ISSN (任意): 1872-9142
ISSN: 0161-5890 (pISSN: 0161-5890, eISSN: 1872-9142)
Title: Molecular immunology
Title(ISO): Mol Immunol
Publisher: Elsevier Ltd.
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2010年 1月 初日 (平成 22年 1月 初日) [継承]
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DOI (任意): 10.1016/j.molimm.2009.10.018    (→Scopusで検索) [継承]
PMID (任意): 19939453    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) Article.Affiliation: Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima, Tokushima 770-8504, Japan. hosokawa@dent.tokushima-u.ac.jp  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
3.(英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]

標準的な表示

和文冊子 ● Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TNFSF14 coordinately enhances CXCL10 and CXCL11 production from IFN-gamma-stimulated human gingival fibroblasts, Molecular Immunology, Vol.47, No.4, 666-670, 2010.
欧文冊子 ● Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : TNFSF14 coordinately enhances CXCL10 and CXCL11 production from IFN-gamma-stimulated human gingival fibroblasts, Molecular Immunology, Vol.47, No.4, 666-670, 2010.

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