Medicine (RMH) - Research Publications

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    MACROPHAGE TUMOR-CELL LINE AND PLASMINOGEN ACTIVATOR - POTENTIAL MODEL SYSTEM FOR MACROPHAGE REGULATION OF ENZYME-PRODUCTION
    HAMILTON, JA ; RALPH, P ; MOORE, MAS (ROCKEFELLER UNIV PRESS, 1978-01-01)
    The macrophage cell line, RAW264.10, synthesizes and secretes plasminogen activator. Production of this enzyme is inhibited by low concentrations of glucocorticoids and increased by phorbol myristate acetate. It is proposed that this line could be a suitable model for the regulation of enzyme synthesis by mouse peritoneal macrophages.
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    MACROPHAGE PLASMINOGEN ACTIVATOR - INDUCTION BY ASBESTOS IS BLOCKED BY ANTI-INFLAMMATORY STEROIDS
    HAMILTON, J ; VASSALLI, JD ; REICH, E (ROCKEFELLER UNIV PRESS, 1976-01-01)
    Intraperitoneal injection of asbestos fibres into mice induces the formation of exudates containing macrophages that produce plasminogen activator. Like-wise, in vitro addition of asbestos to macrophage cultures stimulates plasminogen activator secretion; the synthesis and secretion of lysozyme and lysosomal enzymes are not changed under these conditions. The enhanced secretion of plasminogen activator by macrophages exposed to asbestos is suppressed by low concentrations of anti-inflammatory steroids.
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    Cell-to-cell interaction in the immune response. VII. Requirement for differentiation of thymus-derived cells.
    Miller, JF ; Sprent, J ; Basten, A ; Warner, NL ; Breitner, JC ; Rowland, G ; Hamilton, J ; Silver, H ; Martin, WJ (Rockefeller University Press, 1971-11-01)
    Experiments were designed to test the possibility that thymus-derived (T) cells cooperate with nonthymus derived (B) cells in antibody responses by acting as passive carriers of antigen. Thoracic duct lymphocytes (TDL) from fowl gammaG-tolerant mice were incubated in vitro with fowl anti-mouse lymphocyte globulin (FALG), which was shown not to be immunosuppressive in mice. On transfer into adult thymectomized, irradiated, and marrow protected (TxBM) hosts together with a control antigen, horse RBC, a response to horse RBC but not to fowl gammaG was obtained. By contrast, TxBM recipients of nontolerant, FALG-coated TDL responded to both antigens and the antibody-forming cells were shown to be derived from the host, not from the injected TDL. These findings suggested that, under the conditions of the experiment, triggering of unprimed B cells in the spleens of TxBM hosts was not achieved with antigen-coated tolerant lymphocytes. Another model utilized the ability of B cells to bind antibody-antigen complexes. Spleen cells from TxBM mice, incubated in vitro with anti-fowl gammaG-fowl gammaG.NIP, were injected with or without normal TDL (a source of T cells) into irradiated hosts. Only mice given both cell types could produce an anti-NIP antibody response. In a further experiment, spleen cells from HGG.NIP-primed mice were injected together with NIP-coated B cells (prepared as above) into irradiated hosts. A substantial anti-NIP antibody response occurred. If, however, the T cells in the spleens of HGG.NIP-primed mice were eliminated by treatment with anti-theta serum and complement, the NIP response was abolished. It was concluded that antigen-coated B cells could not substitute for T cells either in the primary or secondary response. Treatment of T cells from unprimed or primed mice with mitomycin C impaired their capacity to collaborate with B cells on transfer into irradiated hosts. Taken together these findings suggest that before collaboration can take place T cells must be activated by antigen to differentiate and in so doing may produce some factor essential for triggering of B cells.