Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.
The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.
D000818:Animals; D000936:Antigen-Antibody Complex; D002450:Cell Communication; D003165:Complement System Proteins; D005260:Female; D006183:H-2 Antigens; D007141:Immunoglobulin Fc Fragments; D007074:Immunoglobulin G; D066298:In Vitro Techniques; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D008954:Models, Biological; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology*
D000936:Antigen-Antibody Complex; D006183:H-2 Antigens; D007141:Immunoglobulin Fc Fragments; D007074:Immunoglobulin G; D003165:Complement System Proteins