The data presented in this paper support the hypothesis that unresponsiveness to autologous thyroglobulin (Tg) exists in the T cells and responsiveness exists in the B cells. Such a conclusion is based on the results of antigen-binding studies where few, if any, thymocytes recognized syngeneic Tg. Comparable numbers of antigen-binding lymphocytes for syngeneic Tg were found in the spleens of normal intact mice and of nude mice. The latter fact suggested that B cells exist which recognize self-constituents. From antigen-suicide experiments, a clearer picture of the susceptibility of B cells to iodinated self-antigen and of the obligatory role of antibody in the induction of lesions was developed. Only bone marrow cells (B cells) were affected by [125I]syngeneic Tg, in which case the incidence of lesions was diminished. From adoptive transfer experiments, the results demonstrate that unresponsiveness may be terminated by immunization with a mixture of heterologous (cross-reacting) Tg's. In this situation T cells are required since a B-cell reconstituted host failed to make antibody (plaque-forming cells) and to develop lesions. T cells in this form of an unresponsive state may recognize determinants on the heterologous Tg unrelated to autologous Tg and as such stimulate the normal complement of B cells to produce antibody that both reacts with autologous and heterologous Tg.

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