Answers are grounded in this paper and cite their sources.
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.
No takes yet. Share an insight, caveat, or question.
Geha et al. (1981) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: