It is possible to regulate the activity of human influenza virus specific helper T-cell clones either by high concentrations of antigen or by anti-idiotypic suppressor T cells. In the absence of accessory cells, the appropriate peptide antigen recognized by the clones induces specific unresponsiveness. This phenomenon, however, is not the result of cytolysis as responsiveness to IL-2 remained unaltered. This suggests that high-dose immunological tolerance need not involve suppressor T cells, and that peptide antigens can interact directly with the T-cell surface. As recent reports suggest that the T-cell surface antigen T3 is involved in the triggering of T lymphocytes and possibly in antigen recognition we have investigated the expression of T3 and other cell surface antigens following the induction of T-cell tolerance. We report here that when a T-cell clone is exposed to a tolerizing concentration of the appropriate peptide antigen, surface T3 antigen is lost in a dose-dependent manner. As loss of surface T3 induced by anti-T3 antibody also results in unresponsiveness to antigen, we conclude that T3 is involved in the process of T-cell triggering by antigen.