The IgE synthesis is regulated by T cell derived IgE-binding factors in an isotype-specific manner. The IgE-potentiating and IgE-suppressive factors may share common structural genes; therefore, a common polypeptide chain and their biologic activities are determined by posttranslational glycosylation processes. Under the physiological conditions, the carbohydrate moieties in the IgE-binding factors formed by a subset of T cells are determined by the ratio between two T cell factors, i.e., glycosylation-enhancing factors and glycosylation-inhibiting factors (GIF), in their environment. GIF is an immunosuppressive lymphokine. Repeated injections of this lymphokine into antigen-primed mice facilitated the generation of antigen-specific suppressor T cells and suppressed both IgE and IgG antibody responses. This effect of GIF was reproduced in vitro. Activation of antigen-specific T cells by antigen-pulsed macrophages, followed by propagation of the antigen-activated T cells by interleukin 2 in the presence of GIF resulted in the generation of suppressor T cells which produced antigen-specific GIF upon antigenic stimulation. Some of the T cell hybridomas constructed from the antigen-specific suppressor T cells formed antigen-specific GIF upon antigenic stimulation. The antigen-specific GIF formed by the T cell hybridoma share several common properties with antigen-specific suppressive factor and suppressed the antibody response of syngeneic mice in a carrier-specific manner. The results obtained with mouse lymphocytes suggest a maneuver to suppress the IgE antibody formation to an allergen in atopic patients.