gp130, The Cytokine Common Signal-Transducer of Interleukin-6 Cytokine Family, Is Downregulated in T Cells In Vivo by Interleukin-6

  • Xue-Jie Wang
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.
  • Tetsuya Taga
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.
  • Kanji Yoshida
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.
  • Mikiyoshi Saito
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.
  • Tadamitsu Kishimoto
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.
  • Hitoshi Kikutani
    From the Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; the Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Co, Ltd, Shizuoka, Japan; and the Department of Medicine III, Osaka University Medical School, Osaka, Japan.

書誌事項

公開日
1998-05-01
DOI
  • 10.1182/blood.v91.9.3308
  • 10.1182/blood.v91.9.3308.3308_3308_3314
公開者
American Society of Hematology

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説明

<jats:title>Abstract</jats:title><jats:p>gp130 is a common signal-transducing receptor component for the interleukin-6 (IL-6) family of cytokines. To investigate the expression of gp130 in T-cell subsets and its regulation, anti-murine gp130 monoclonal antibody (MoAb) was used for flow cytometric analysis. In normal mice, gp130 was differentially expressed in thymocyte and splenic T-cell subpopulations defined by CD4/CD8 expression. In aged MRL/lpr mice, although gp130 expression was detectable in splenic CD4+ or CD8+ T cells, gp130 expression was significantly downregulated. Because serum levels of IL-6 and soluble IL-6 receptor (sIL-6R) are elevated in these mice, we examined the possibility that the downregulation of gp130 expression on splenic T cells might be produced in response to continuous activation of gp130 by high levels of serum IL-6. In transgenic mice overexpressing IL-6, gp130 expression in the splenic T cells was significantly decreased. After stimulation with IL-6 in vitro, the level of gp130 on CD4+ or CD8+ splenic T cells from normal mice was significantly decreased. These results suggest that the expression of gp130 in splenic T cells could be downregulated by the IL-6 stimulation under physiological or pathological circumstances.</jats:p>

収録刊行物

  • Blood

    Blood 91 (9), 3308-3314, 1998-05-01

    American Society of Hematology

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