Antigen-Macrophage Interaction

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Abstract
Antigen-stimulated tritiated thymidine (3H-TdR) incorporation by lymphocytes is an in vitro correlate of cellular immunity. The stimulation of this response by hapten-carrier conjugates may be inhibited by free hapten, a finding previously interpreted as evidence for independent hapten-specificity of thymus dependent (T) lymphocyte receptors. We confirm the specific inhibition by dinitrophenyl (DNP)-lysine of DNP-guinea pig albumin (GPA) induced stimulation of lymphoid cell cultures from guinea pigs immunized with DNP-GPA and report a similar specific inhibition caused by DNP-ovalbumin (OVA). Nonetheless, our results indicate that this hapten-specific inhibition is not due to blockade of T cell receptors specific for hapten-carrier conjugates. Thus we show: 1) DNP-OVA must be present before and during “pulse” exposure to DNP-GPA but has no effect if added after such a pulse. 2) Preincubation of macrophage-rich peritoneal exudate cells with DNP-OVA blocks the capacity of these cells to bind low concentrations of DNP-GPA and then to stimulate immune peritoneal exudate lymphocytes to divide. 3) Preincubation of DNP-GPA immune peritoneal exudate lymphocytes in DNP-OVA has no effect on their capacity to subsequently respond to macrophage-associated DNP-GPA. We conclude that the capacity of DNP-OVA to inhibit DNP-GPA stimulation of 3H-TdR incorporation by lymphoid cell populations from guinea pigs immune to DNP-GPA is due to competition for a hapten-specific cytophilic antibody on the surface of the macrophage and not to competition for a hapten-specific receptor on T lymphocytes.

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