Abstract
Certain aspects of the phenomenon of IgE class-restricted tolerance induced in mice by neonatal treatment with monoclonal IgE, in soluble form or coupled to syngeneic spleen cells, were examined. This tolerance apparently results from exposure to IgE molecules, irrespective of their antigen specificity, and the resulting effects are polyclonal in nature since IgE responses directed against antigenic determinants unrelated to the tolerance-inducing IgE molecules are affected. By analyzing the lymphoid cells of IgE-tolerant mice after they reached adulthood, the following observations were made: lymphoid cells from such tolerant mice failed to develop FcR.epsilon.+ cells upon in vitro stimulation with IgE, as is characteristically observed with lymphoid cells from nontolerant mice; and mice rendered tolerant by neonatal treatment with soluble IgE possess IgE class-restricted suppressor T cells, demonstrable in adoptive transfer experiments, whereas no such suppressor cells are evident in mice in which cell-bound IgE was used for neonatal treatment. Two different mechanisms could underlie the IgE class-restricted tolerance, both mechanisms operate coordinately to varying degrees depending upon which regimen is used for tolerance induction.