Abstract

Previous experiments on the regulation of the IgE response in BDF1 mice provided a method of generating antigen specific suppressor T cells in vitro from antigen primed T cell populations [1]. Spleen cells of BDF1 mice primed with alum absorbed ovalbumin (OVA) for a persistent IgE response produced IgE potentiating factors, i.e., glycosylated IgE binding factors (IgE-BF) after antigenic stimulation but did not contain antigen-specific suppressor cells [2]. However, propagation of the antigen-activated T cells by interleukin-2 (IL-2) in the presence of glycosylation inhibiting factor (GIF) [3] or synthetic phospholipase A2 inhibitor facilitated the generation of antigen specific T cells that produced their own GIF. Stimulation of the T cells with OVA-pulsed syngeneic macrophages resulted in the formation of an IgE suppressive factor, i.e., unglycosylated IgE-BF and GIF, the latter of which had affinity for OVA. Thus, T cell hybridomas were constructed from the OVA specific T cells. Upon antigenic stimulation, some of the hybridomas formed OVA-binding GIF, which suppressed the primary IgE response of BDF 1 mice to dinitrophenol (DNP)-OVA in a carrier specific manner [4] and which shared common antigenic structures with effector type, antigen specific, suppressor T cell factor (TseF) [5].

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