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Experiments presented in this report demonstrate that specificity of the Ly1+ T cell proliferative response to NP-modified Ig is controlled by Igh-C-linked genes. In addition, we describe the mechanism whereby Igh-C-encoded molecules influence Ly1+ T cell activity. We show that Igh-C-linked control of T cell responses to NP-modified Ig is a secondary consequence of naturally acquired tolerance for self Ig. Unresponsiveness to self Ig is not due to a defect expressed functionally at the level of the antigen-presenting cell, nor is it associated with active suppression. These results suggest that tolerance for self Ig at the level of the Ly1+ T cell is due to functional deletion of Ly1+ T cell clones specific for self Ig. The possibility is considered that regulatory effects mediated by passively administered antibodies may in part be due to induction of Ly1+ T cell tolerance for self Ig.


Journal article


J Exp Med

Publication Date





1868 - 1880


Animals, Antigens, Ly, Immune Tolerance, Immunoglobulin Heavy Chains, Immunoglobulins, Lymphocyte Activation, Major Histocompatibility Complex, Mice, Mice, Inbred BALB C, Nitrophenols, Phenylacetates, T-Lymphocytes, Trinitrobenzenes