Adsorption of T cells over monolayers of autologous, but not allogeneic, macrophages (M phi) pulsed with tetanus toxoid (TT) antigen resulted in the specific depletion of the capacity of the T cells to proliferate and to release T cell helper factor in response to stimulation, with TT antigen. T cells that bound to the TT-pulsed M phi monolayers were specifically enriched in their capacity to proliferate in response to TT. Turkey antiserum to the human B cell glycoprotein p 29,34, but not turkey antiserum to human beta 2 microglobulin, inhibited the binding of TT-reactive T cells to TT-pulsed M phi. This inhibition resulted from the binding of the anti-p 29,34 antiserum to DR determinants expressed on the surface of the M phi. Immunosorbent purified IgG anti-TT, added in great excess, did not inhibit the binding of TT-reactive T cells to TT-pulsed M phi monolayers. Soluble TT antigen and rabbit antiidiotypic IgG, directed against IgG F(ab')2 anti-TT obtained from the cell donor, minimally inhibited the binding of TT-reactive T cells to TT pulsed M phi monolayers. M phi pulsed with urea-denatured TT, which contained less than 1% native TT, depleted T cell reactivity to TT to an extent almost equivalent to that achieved by M phi pulsed with native TT. These results indicate that human antigen-reactive T cells bind to the DR determinants of M phi pulsed with antigen and that the immunogenic moiety of antigen recognized by the majority of antigen reactive human T cells may differ from native antigen.

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