『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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登録内容 (EID=98385)

EID=98385EID:98385, Map:0, LastModified:2014年2月28日(金) 13:52:59, Operator:[大家 隆弘], Avail:TRUE, Censor:0, Owner:[石丸 直澄], 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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カテゴリ (推奨):
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組織 (推奨):
著者 (必須): 1. (英) Saegusa Kaoru (日) (読)
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2.石丸 直澄 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学])
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3. (英) Yanagi Kumiko (日) (読)
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4. (英) Mishima Kenji (日) (読)
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5.新垣 理恵子 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学])
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6. (英) Suda Takashi (日) (読)
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7. (英) Saito Ichiro (日) (読)
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8.林 良夫
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題名 (必須): (英) Prevention and induction of autoimmune exocrinopathy is dependent on pathogenic autoantigen cleavage in murine Sjogren's syndrome  (日)    [継承]
副題 (任意):
要約 (任意): (英) The in vivo role of autoantigen cleavage during apoptosis in autoimmune diseases remains unclear. Previously, we found a cleavage product of 120-kDa alpha-fodrin as an important autoantigen in the pathogenesis of primary Sjögren's syndrome (SS). In the murine primary SS model, tissue-infiltrating CD4(+) T cells purified from the salivary glands bear a large proportion of Fas ligand, and the salivary gland duct cells constitutively possess Fas. Infiltrating CD4(+) T cells, but not CD8(+) T cells, identified significant (51)Cr release against mouse salivary gland cells. In vitro studies demonstrated that apoptotic mouse salivary gland cells result in a specific alpha-fodrin cleavage into 120 kDa and that preincubation with caspase inhibitor peptides blocked alpha-fodrin cleavage. In vivo treatment with caspase inhibitors N-benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone and N-acetyl-Asp-Glu-Val-Asp-al-CHO into the murine model results in dramatic inhibitory effects on the development of autoimmune lesions and in restoration of sicca syndrome. Furthermore, we found that immunization with recombinant alpha-fodrin protein identical with an autoantigen into normal recipients induced autoimmune lesions similar to SS. These data indicate that prevention and induction of autoimmune exocrinopathy is dependent on autoantigen cleavage via caspase cascade and that caspase inhibitors might provide a new therapeutic option directed at reducing tissue damage in the murine model for SS.  (日)    [継承]
キーワード (推奨): 1. (英) NONERYTHROID ALPHA-SPECTRIN (日) (読) [継承]
2. (英) FAS-MEDIATED APOPTOSIS (日) (読) [継承]
3. (英) ICE (日) (読) [継承]
4. (英) CED-3 PROTEASE (日) (読) [継承]
5. (英) POLY(ADP-RIBOSE) POLYMERASE (日) (読) [継承]
6. (英) CPP32-LIKE PROTEASES (日) (読) [継承]
7. (英) MOUSE MODEL (日) (読) [継承]
8. (英) FODRIN (日) (読) [継承]
9. (英) CELLS (日) (読) [継承]
10. (英) MICE (日) (読) [継承]
11. (英) ACTIVATION (日) (読) [継承]
発行所 (推奨):
誌名 (必須): The Journal of Immunology ([The American Association of Immunologists])
(pISSN: 0022-1767, eISSN: 1550-6606)

ISSN (任意): 0022-1767
ISSN: 0022-1767 (pISSN: 0022-1767, eISSN: 1550-6606)
Title: Journal of immunology (Baltimore, Md. : 1950)
Title(ISO): J Immunol
Publisher: American Association of Immunologists
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 169 [継承]
(必須): 2 [継承]
(必須): 1050 1057 [継承]
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年月日 (必須): 西暦 2002年 5月 3日 (平成 14年 5月 3日) [継承]
URL (任意): http://ci.nii.ac.jp/naid/80015444001/ [継承]
DOI (任意):
PMID (任意): 12097413    (→Scopusで検索) [継承]
NAID (任意): 80015444001 [継承]
WOS (任意): 000176753500052 [継承]
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備考 (任意): 1.(英) Article.Affiliation: Department of Pathology, Tokushima University School of Dentistry, Tokushima, Japan.  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Kaoru Saegusa, Naozumi Ishimaru, Kumiko Yanagi, Kenji Mishima, Rieko Arakaki, Takashi Suda, Ichiro Saito and Yoshio Hayashi : Prevention and induction of autoimmune exocrinopathy is dependent on pathogenic autoantigen cleavage in murine Sjogren's syndrome, The Journal of Immunology, Vol.169, No.2, 1050-1057, 2002.
欧文冊子 ● Kaoru Saegusa, Naozumi Ishimaru, Kumiko Yanagi, Kenji Mishima, Rieko Arakaki, Takashi Suda, Ichiro Saito and Yoshio Hayashi : Prevention and induction of autoimmune exocrinopathy is dependent on pathogenic autoantigen cleavage in murine Sjogren's syndrome, The Journal of Immunology, Vol.169, No.2, 1050-1057, 2002.

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