『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=249013EID:249013, Map:0, LastModified:2013年7月19日(金) 18:31:43, 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]
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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. (英) Shindo Satoru (日) 進藤 智 (読) しんどう さとる
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4.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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5.中江 英明
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6.松尾 敬志
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題名 (必須): (英) Tumor necrosis factor-like weak inducer of apoptosis increases CC chemokine ligand 20 production in interleukin 1-stimulated human gingival fibroblasts.  (日)    [継承]
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要約 (任意): (英) CC chemokine ligand 20 (CCL20) is related to T-helper (Th)-17 cell migration, and Th17 cells play important roles in exacerbation in periodontal disease. However, the effect of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) on CCL20 production is unknown. In this study, we examined the mechanisms of TWEAK in combination with interleukin (IL)-1-induced CCL20 production in human gingival fibroblasts (HGFs). TWEAK alone did not induce CCL20 production in HGFs. However, TWEAK enhanced CCL20 expression from IL-1-stimulated HGFs in a dose-dependent manner. Inhibitors of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK), protein kinase B (Akt), and nuclear factor B (NF-B) significantly inhibited CCL20 production in TWEAK and IL-1-stimulated HGFs. Western blot analysis revealed that phosphorylations of ERK, Akt, and inhibitor of NF-B were enhanced in TWEAK and IL-1-treated HGFs. These data suggest that TWEAK is positively related to Th17 cell migration in periodontally diseased tissues to enhance CCL20 production in IL-1-stimulated HGFs.  (日)    [継承]
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誌名 (必須): Human Immunology (American Association of Clinical Histocompatibility Testing/American Society for Histocompatibility and Immunogenetics)
(pISSN: 0198-8859, eISSN: 1879-1166)

ISSN (任意): 1879-1166
ISSN: 0198-8859 (pISSN: 0198-8859, eISSN: 1879-1166)
Title: Human immunology
Title(ISO): Hum Immunol
Publisher: Elsevier BV
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 470 473 [継承]
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年月日 (必須): 西暦 2012年 3月 6日 (平成 24年 3月 6日) [継承]
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DOI (任意): 10.1016/j.humimm.2012.02.021    (→Scopusで検索) [継承]
PMID (任意): 22425737    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) Affiliation: Department of Conservative Dentistry, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8504, Japan. hosokawa@dent.tokushima-u.ac.jp  (日)    [継承]
2.(英) PublicationType: Journal Article  (日)    [継承]
3.(英) 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, Satoru Shindo, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Tumor necrosis factor-like weak inducer of apoptosis increases CC chemokine ligand 20 production in interleukin 1-stimulated human gingival fibroblasts., Human Immunology, Vol.73, No.5, 470-473, 2012.
欧文冊子 ● Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Tumor necrosis factor-like weak inducer of apoptosis increases CC chemokine ligand 20 production in interleukin 1-stimulated human gingival fibroblasts., Human Immunology, Vol.73, No.5, 470-473, 2012.

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