Macrophage support and suppression in rabbit T cell mitogenesis.
The role of macrophages in mitogen-induced rabbit T cell proliferation has been investigated. The blastogenic response to the 3 mitogens, PHA, ConA and oxidative treatment by neuraminidase and galactose oxidase (NaGo) was tested. T cell proliferation was reduced by removal of low density or plastic adherent cells, including macrophages, and could be enhanced by the addition of peritoneal resident macrophages, indicating a macrophage requirement for rabbit T cell proliferation. However, PHA-induced proliferation could not be raised to the level expected. It was found that catalase and especially 2-ME could considerably enhance macrophage dependent proliferation, even at low macrophage concentrations. It is concluded therefore, that macrophages not only support but also suppress lymphocyte proliferation, namely by non-specific damage to lymphocytes through release of radicals and hydrogen peroxide. In addition, peritoneal, but not lymph node macrophages were found to suppress lymphocyte proliferation by prostaglandin production, although to a lesser extent. Experiments, done in the presence of blockers of macrophage-mediated suppression, showed that macrophages were able to magnify the PHA-induced T cell proliferation to the expected values. The experiments thus show that unactivated macrophages support and suppress lymphocyte proliferation at the same time.
D000818:Animals; D002374:Catalase / Q000494:pharmacology; D002469:Cell Separation; D005260:Female; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D007213:Indomethacin / Q000494:pharmacology; D008198:Lymph Nodes / Q000166:cytology; D008213:Lymphocyte Activation / Q000187:drug effects; D008264:Macrophages / Q000276:immunology*; D008623:Mercaptoethanol / Q000494:pharmacology; D008934:Mitogens / Q000494:pharmacology; D011817:Rabbits; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D008934:Mitogens; D008623:Mercaptoethanol; D002374:Catalase; D007213:Indomethacin