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Antigen-Macrophage Interaction

I. Hapten-Specific Inhibition of Antigen Interaction with Macrophages from Immune Animals

From the Laboratory of Immunology and Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014

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.