Requirement for MD-1 in cell surface expression of RP105/CD180 and B-cell responsiveness to lipopolysaccharide

DOI PDF 被引用文献17件
  • Yoshinori Nagai
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Rintaro Shimazu
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Hirotaka Ogata
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Sachiko Akashi
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Katsuko Sudo
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Hidetoshi Yamasaki
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Shin-Ichi Hayashi
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Yoichiro Iwakura
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Masao Kimoto
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.
  • Kensuke Miyake
    From the Department of Immunology, Saga Medical School, Japan; the Center for Experimental Medicine, Division of Infectious Genetics, The Institute of Medical Science, The University of Tokyo, Japan; and the Department of Immunology, Faculty of Medicine, Tottori University, Yonago, Japan.

抄録

<jats:p>RP105 is a B-cell surface molecule that has been recently assigned as CD180. RP105 ligation with an antibody induces B-cell activation in humans and mice, leading to proliferation and up-regulation of a costimulatory molecule, B7.2/CD86. RP105 is associated with an extracellular molecule, MD-1. RP105/MD-1 has structural similarity to Toll-like receptor 4 (TLR4)/MD-2. TLR4 signals a membrane constituent of Gram-negative bacteria, lipopolysaccharide (LPS). MD-2 is indispensable for TLR4-dependent LPS responses because cells expressing TLR4/MD-2, but not TLR4 alone, respond to LPS. RP105 also has a role in LPS responses because B cells lacking RP105 show hyporesponsiveness to LPS. Little is known, however, regarding whether MD-1 is important for RP105-dependent LPS responses, as MD-2 is for TLR4. To address the issue, we developed mice lacking MD-1 and generated monoclonal antibodies (mAbs) to the protein. MD-1–null mice showed impairment in LPS-induced B-cell proliferation, antibody production, and B7.2/CD86 up-regulation. These phenotypes are similar to those of RP105-null mice. The similarity was attributed to the absence of cell surface RP105 on MD-1–null B cells. MD-1 is indispensable for cell surface expression of RP105. A role for MD-1 in LPS responses was further studied with anti–mouse MD-1 mAbs. In contrast to highly mitogenic anti-RP105 mAbs, the mAbs to MD-1 were not mitogenic but antagonistic on LPS-induced B-cell proliferation and on B7.2 up-regulation. Collectively, MD-1 is important for RP105 with respect to B-cell surface expression and LPS recognition and signaling.</jats:p>

収録刊行物

  • Blood

    Blood 99 (5), 1699-1705, 2002-03-01

    American Society of Hematology

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