Evidence for direct control of an in vitro plaque-forming cell response by quantitative properties of intact, fluid, haptenated liposomes: a potential model system for antigen presentation by macrophages.

Stimulation of the primary in vitro plaque-forming cell (PFC)2 response to fluid, haptenated liposomes by spleen cells depleted of a Sephadex-adherent population has been made possible by the addition of an uncharacterized cell-derived soluble factor(s). In its absence, PFC responses by such cells are greatly reduced or absent. The factor(s) is present in the supernatant from Concanavalin A-stimulated spleen cells. This phenomenon has permitted a comparison of the behavior of cultures with and without adherent cells, with a view to determining the relative likelihood of liposomes or adherent cells functioning as antigen presenters in this system. Two modes of control by quantitative properties of liposomes have been studied. PFC stimulation is controlled, in a biphasic manner, by varying either liposomal epitope density at constant liposome concentration or liposome concentration at fixed epitope density. Overall hapten concentration in the cultures is only of significance as a consequence of epitope density and liposome concentration; it does not, itself, control the response. Whole spleen cell cultures and cultures depleted of Sephadex-adherent cells but supplemented with soluble factor(s) exhibit the same biphasic response profiles when these quantitative properties of liposomes are varied. The results argue against the role of Sephadex-adherent cells as antigen presenters in whole spleen cell cultures. A model in which antigen presentation is accomplished by intact liposomes, in both whole spleen and adherent cell-depleted cultures, is consistent with the data.