Alpha-galactosylceramide によるiNKT 細胞活性化と肝傷害  [in Japanese] Liver Injury and Invariant NKT Cells Activation by Alpha-galactosylceramide  [in Japanese]

Access this Article

Search this Article

Author(s)

    • 長谷川 寛 Hasegawa Hiroshi
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 掛地 吉弘 Kakeji Yoshihiro
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 山下 公大 Yamashita Kimihiro
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 西 将康 Nishi Masayasu
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 田中 智子 Tanaka Tomoko
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 有本 聡 Arimoto Satoshi
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 松田 武 Matsuda Takeru
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 角 泰雄 Sumi Yasuo
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 中村 哲 Nakamura Tetsu
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
    • 鈴木 知志 Suzuki Satoshi
    • 神戸大学大学院 食道胃腸外科学分野 Department of Surgery, Division of Gastrointestinal Surgery, Kobe University Graduate School of Medicine, Kobe, Japan

Abstract

<p>Both free alpha-galactosylceramide (αGalCer) and αGalCer loaded dendritic cells (DCG) activate invariant NaturalKiller T (iNKT) cells. Interestingly, although both free αGalCer and DCG treatment induce liver injury, DCG treatment doesn't cause lethal liver injury compared with free αGalCer treatment. DCG may be able to activate iNKT cells directly <i>in vivo</i>. On the other hand, free αGalCer are taken by CD1d-positive cells and CD1d-positive cells present CD1d-αGalCer complex for iNKT cells <i>in vivo</i>. Specialized antigen-presenting cells such as dendritic cells may play antigen presentation for iNKT cells, however, how other CD1d positive cells participate in this reaction is not clear. Using CD31 antibody and sorting technique, we separate CD31 negative hepatocyte (HC) and CD31 positive endothelial cells (EC). Both CD31 negative HC and CD31 positive EC are CD1d-positive cells. We showed that CD31 positive EC were more injured after free αGalCer treatment than after DCG treatment. Moreover, EC from mice treated with free αGalCer induced naïve hepatic lymphocyte to produce TNF, which play pivotal role in liver injury by both free αGalCer and DCG treatment, and EC from mice treated with DCG did not. These results indicate that EC play antigen presentation for iNKT cells after free αGalCer treatment and injury of EC may relate to lethal liver injury.</p>

Journal

  • Cytometry Research

    Cytometry Research 26(2), 21-25, 2016

    Japan Cytometry Society

Codes

Page Top