Abstract
Over the last several years our laboratory has been engaged in the in vitro study of the regulation of IgE synthesis. We have found that polyclonal B cell activators fail to induce IgE synthesis in human B cells. Alloreactive T cell helper clones induced synthesis in B cells only under conditions of interaction and in B cells from allergic donors under cognate conditions of bystander stimulation as well. Isotype-specific regulation of the IgE response was mediated in the secretion of IgE-binding factors by T cells suppressing Fc receptors for IgE. Finally, IgE immune complexes in sera from patients with hyper-IgE states were shown to downregulate T cell proliferation to antigen and to stimulate monocytes to resorb 45Ca-labelled bone and to release prostaglandins. The implications of these in vitro findings for disease states in which IgE is elevated are discussed.
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