Comparison of the expression of IL 2 receptors by human T and B cells: induction by the polyclonal mitogens, phorbol myristate acetate, and anti-mu antibody.
It is well established that IL 2 plays an important role in the proliferative response of T cells. Activated B cells were also recently found to express IL 2 receptors. The present studies were designed to compare qualitative, quantitative, and functional aspects of IL 2 receptor expression by activated T and B cells. Phorbol myristate acetate (PMA)-activated human T and small resting B cells and enhanced the expression of HLA-DR, HLA-DC/DS, and transferrin receptors while reducing Leu-4 antigen expression by T cells and IgM and IgD expression on B cells. PMA induced both T and B cells to express functional IL 2 receptors before cellular proliferation. Immune interferon did not participate in this induction. The m.w. of the IL 2 receptors expressed by activated T and B cells was identical: 54,000 to 59,000. Several differences were noted in the expression of IL 2 receptors by activated T and B cells on stimulation with PMA; T cells expressed IL 2 receptors sooner than B cells and in higher density, and the enhanced proliferative response of T cells to IL 2 was more difficult to inhibit with antibody to IL 2 receptors. In addition, IL 2 enhanced the expression of transferrin receptors by activated T cells but did not have a similar effect on activated B cells. Small B cells from the blood could also be induced by a mitogenic monoclonal anti-IgM antibody to express functional IL 2 receptors. Relatively large B cells in fresh blood samples were found to express functional IL 2 receptors and were capable of a modest proliferative response to IL 2. The intensity of the IL 2 receptor expression and the proliferative response by large B cells were enhanced by PMA stimulation. The data suggest that IL 2 receptors may play an auxiliary role in the B cell proliferative response and that IL 2 may exert its effect at a late phase in the B cell activation process.
Suzuki
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Cooper
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D000911:Antibodies, Monoclonal / Q000502:physiology; D000954:Antigens, Surface / Q000032:analysis / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D001667:Binding, Competitive; D004306:Dose-Response Relationship, Immunologic; D004357:Drug Synergism; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology; D007700:Kinetics; D007958:Leukocyte Count; D008213:Lymphocyte Activation / Q000187:drug effects; D008934:Mitogens / Q000494:pharmacology*; D008970:Molecular Weight; D010704:Phorbols / Q000494:pharmacology*; D011956:Receptors, Cell Surface / Q000032:analysis; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000187:drug effects / Q000502:physiology; D015375:Receptors, Interleukin-2; D011990:Receptors, Transferrin; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; D000511:alpha-Macroglobulins / Q000494:pharmacology*
D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D007075:Immunoglobulin M; D008934:Mitogens; D010704:Phorbols; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D011990:Receptors, Transferrin; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; D000511:alpha-Macroglobulins; C032306:polyclonal B cell activator; D013755:Tetradecanoylphorbol Acetate