Abstract
It is possible to regulate the activity of human influenza virus specific helper T-cell clones either by high concentrations of antigen1 or by anti-idiotypic suppressor T cells2. 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 respon-siveness 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 recognition3,4 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.
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Zanders, E., Lamb, J., Feldmann, M. et al. Tolerance of T-cell clones is associated with membrane antigen changes. Nature 303, 625–627 (1983). https://doi.org/10.1038/303625a0
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DOI: https://doi.org/10.1038/303625a0
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