Rheumatoid Factor Secretion from Human Leu-1 <sup>+</sup> B Cells

  • Richard R. Hardy
    Institute for Molecular and Cellular Biology, Osaka University, 1-3, Yamada-Oka, Suita, Osaka 565, Japan.
  • Kyoko Hayakawa
    Institute for Molecular and Cellular Biology, Osaka University, 1-3, Yamada-Oka, Suita, Osaka 565, Japan.
  • Masatoshi Shimizu
    Osaka-Minami National Hospital, Kawachi- nagano, Osaka 586, Japan.
  • Katsuhiko Yamasaki
    Institute for Molecular and Cellular Biology, Osaka University, 1-3, Yamada-Oka, Suita, Osaka 565, Japan.
  • Tadamitsu Kishimoto
    Institute for Molecular and Cellular Biology, Osaka University, 1-3, Yamada-Oka, Suita, Osaka 565, Japan.

抄録

<jats:p> A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1 (CD5) is responsible for most of the immunoglobulin M rheumatoid factor secreted in vitro after the cells are stimulated with <jats:italic>Staphylococcus aureus</jats:italic> . The ability of B cells bearing the Leu-1 marker (Leu-1 <jats:sup>+</jats:sup> ) to secrete rheumatoid factor is present early in development and extends to adulthood, since Leu-1 <jats:sup>+</jats:sup> B cells from cord blood and from peripheral blood lymphocytes of both normal adults and patients with certain autoimmune conditions secrete rheumatoid factor in comparable amounts. The neonatal enrichment of Leu-1 <jats:sup>+</jats:sup> B cells, the presence of Leu-1 <jats:sup>+</jats:sup> B cells in increased frequencies in patients with autoimmune disease, and the involvement of Leu-1 <jats:sup>+</jats:sup> B cells in autoantibody secretion suggest both developmental and functional homologies between this human B cell subpopulation and the murine Ly-1 B cell subpopulation. </jats:p>

収録刊行物

  • Science

    Science 236 (4797), 81-83, 1987-04-03

    American Association for the Advancement of Science (AAAS)

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