Nature of the antigenic complex recognized by T lymphocytes. VIII. Specific inhibition of the stimulatory capacity of antigen‐pulsed hapten‐modified peritoneal exudate cells by anti‐hapten antibody

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Abstract
When macrophages which were pulsed with soluble protein antigens and then modified with 2,4,6-trinitrobenzenesulfonic acid (TNBS) were cultured with primed T cells in the presence of anti-2,4,6-trinitrophenyl (TNP) antiserum, a marked inhibition of the T cell proliferative response specific for the soluble protein antigen under study was observed. Inhibition of the proliferative response required that the protein antigen under study be easily susceptible to conjugation with TNBS. A lag period of 1-3 h must elapse following pulse exposure to the protein antigen and prior to TNP modification for anti-TNP antibody to exert an inhibitory effect, which suggests that processing of antigen in an intracellular site might occur with subsequent reexpression of antigen on the macrophage surface. It was hypothesized that anti-TNP antibody inhibits T cell proliferation by capping and shedding of TNP-modified determinants of the nominal antigen as well as TNP-modified cell surface proteins from the macrophage membrane. The failure of others to demonstrate an effect of anti-antigen antibody on T cell activation can best be explained as secondary to the low density of antigenic determinants on the macrophage membrane with resultant low-affinity binding of antibody to antigen.