The data presented herein indicate that IgE synthesis results from a complex interaction between T cells, B cells, and monocytes, under the control of T cell-derived and monocyte-derived lymphokines (IL-4, IL-5, and IL-6). In addition to their direct effects on IgE synthesis, these lymphokines have other functions, many of which are related to IgE. IL-4 is not only a crucial signal for the induction of IgE synthesis, but also a growth factor for murine mast cells together with IL-3, a product of the same T cell clones. Furthermore, IL-4 is a potent inducer of Fc epsilon R2b expression on both B cells and monocytes. On the other hand, IL-4-secreting T cells also produce IL-5, which promotes B cell maturation and induces differentiation of eosinophil precursors. Eosinophils, in turn, express CD23 when activated; thus, the activation of the IgE system leads to increased IgE synthesis and to enhanced expression of Fc epsilon R1 (on mast cells) and Fc epsilon R2 (on B cells, monocytes, and eosinophils). This in turn results in increased receptor-ligand interactions, with release of different chemical mediators involved in the pathogenesis of allergy. Such considerations suggest that the regulation of IgE synthesis should be viewed in the wider context of the IgE system, a multi-component network in which different cell types are functionally integrated mainly through lymphokine-mediated signals.(ABSTRACT TRUNCATED AT 250 WORDS)