CD23/IgE-mediated regulation of the specific antibody response in vivo.

Abstract We have recently reported that IgE Abs specific for TNP are able to enhance the specific IgG response in mice via the low affinity receptor for IgE, Fc epsilon RII, or CD23. In this study we show that IgE can up-regulate IgM, IgG1, IgG2a, and the IgE response, thereby indicating the possibility of a viscious circle in the maintenance of an allergic response. One of the suggested modes of action of IgE/CD23 is to increase the ability of B cells to present Ag to T cells. The involvement of T cells in IgE-mediated enhancement of the Ab response was studied in several ways: nude mice were resistant to the effect of IgE and a dramatic effect on the induction of immunologic memory was seen, both by in situ secondary immunizations and in adoptive transfer systems. Basic conditions for the ability of IgE to induce enhancement were established, demonstrating critical importance of factors such as type of Ag and temporal relationship between administration of IgE and Ag. Finally, no evidence for the requirement for CD23 for a normal (non-IgE induced) Ab response was found, although modulation of the receptor completely abrogated the IgE-induced Ab response.