Tolerance for self IG at the level of the Ly1+ T cell.

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Abstract
Experiments presented in this report demonstrate that specificity of the Lyl+ T cell proliferative response [in mice] to NP[(4-hydroxy-3-nitrophenyl)acetyl]-modified Ig is controlled by Igh-C-linked genes. The mechanism whereby Igh-C- encoded molecules influence Lyl+ T cell activity is described. 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. Evidently, tolerance for self Ig at the level of the Lyl+ T cell is due to functional deletion of Lyl+ 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 Lyl+ T cell tolerance for self Ig.