徳島大学 教育・研究者情報データベース(EDB)

Education and Research Database (EDB), Tokushima University

徳島大学ウェブサイトへのリンク

著作: Zhang W/Moritoki Y/[常山 幸一]/Yang G-X/Ilan Y/Lian Z-X/Gershwin M E/Beta-glucosylceramide ameliorates liver inflammation in murine autoimmune cholangitis./[Clinical and Experimental Immunology]

ヘルプを読む

「著作」(著作(著書,論文,レター,国際会議など))は,研究業績にかかる著作(著書,論文,レター,国際会議など)を登録するテーブルです. (この情報が属するテーブルの詳細な定義を見る)

  • 項目名の部分にマウスカーソルを置いて少し待つと,項目の簡単な説明がツールチップ表示されます.

この情報をEDB閲覧画面で開く

EID
372053
EOID
994870
Map
0
LastModified
2020年10月30日(金) 19:29:31
Operator
大家 隆弘
Avail
TRUE
Censor
0
Owner
常山 幸一
Read
継承
Write
継承
Delete
継承
種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. (英) Zhang W
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Moritoki Y
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. 常山 幸一([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.疾患病理学])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Yang G-X
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Ilan Y
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. (英) Lian Z-X
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. (英) Gershwin M E
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Beta-glucosylceramide ameliorates liver inflammation in murine autoimmune cholangitis.

副題 任意
要約 任意

(英) We have demonstrated spontaneous development of autoimmune cholangitis, similar to human primary biliary cirrhosis, in mice expressing a dominant negative form of the transforming growth factor-beta receptor (dnTGF-betaRII) restricted to T cells. The autoimmune cholangitis appears to be mediated by autoreactive CD8(+) T lymphocytes that home to the portal tracts and biliary system. Because the liver pathology is primarily secondary to CD8(+) T cells, we have determined herein whether administration of beta-glucosylceramide (GC), a naturally occurring plant glycosphingolipid, alters the natural history of disease in this model. We chose GC because previous work has demonstrated its ability to alter CD8(+) T cell responses and to down-regulate tissue inflammation. Accordingly, dnTGF-betaRII mice were treated with either GC or control for a period of 18 weeks beginning at 6 weeks of age. Importantly, in mice that received GC, there was a significant decrease in the frequency and absolute number of autoreactive liver-infiltrating CD8(+) T cells, accompanied by a significant decrease in activated CD44(high) CD8(+) T cell populations. Further, there was a significant reduction in portal inflammation in GC-treated mice. Interestingly, there were no changes in anti-mitochondrial antibodies, CD4(+) T cells, CD19(+) B cells or natural killer (NK) T cell populations, indicating further that the beneficial effects of GC on liver inflammation were targeted specifically to liver-infiltrating CD8(+) T cells. These data suggest that further work on GC in models of CD8(+) T-mediated inflammation are needed and point to a new therapeutic venue for potentially treating and/or modulating autoimmune disease.

キーワード 推奨
  1. (英) Animals
  2. (英) Autoimmune Diseases
  3. (英) CD8-Positive T-Lymphocytes
  4. (英) Cholangitis
  5. (英) Flow Cytometry
  6. (英) Glucosylceramides
  7. (英) Liver
  8. (英) Liver Cirrhosis, Biliary
  9. (英) Mice
  10. (英) Mice, Transgenic
  11. (英) Models, Animal
  12. (英) Protein-Serine-Threonine Kinases
  13. (英) Receptor, Transforming Growth Factor-beta Type II
  14. (英) Receptors, Transforming Growth Factor beta
発行所 推奨
誌名 必須 Clinical and Experimental Immunology(British Society for Immunology)
(pISSN: 0009-9104, eISSN: 1365-2249)
ISSN 任意 1365-2249
ISSN: 0009-9104 (pISSN: 0009-9104, eISSN: 1365-2249)
Title: Clinical and experimental immunology
Title(ISO): Clin Exp Immunol
Supplier: British Society for Immunology
Publisher: Wiley Publishing
 (NLM Catalog  (Wiley  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 157
必須 3
必須 359 364
都市 任意
年月日 必須 2009年 9月 初日
URL 任意
DOI 任意 10.1111/j.1365-2249.2009.03971.x    (→Scopusで検索)
PMID 任意 19664143    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) PublicationType: Journal Article

  2. (英) PublicationType: Research Support, N.I.H., Extramural

  3. (英) PublicationType: Research Support, Non-U.S. Gov't