ADMINISTRATION OF AN ANTI-IGE ANTIBODY INHIBITS CD23 EXPRESSION AND IGE PRODUCTION IN-VIVO

High IgE responder BDF1 mice were immunized intraperitoneally (i.p.) w ith dinitrophenol(4) (DNP4)-ovalbumin (OVA) in alum concomitant with i ntravenous (i.v.) administration of an anti-IgE monoclonal antibody (m Ab). IgE levels were undetectable in mice treated with the anti-IgE an tibody, whereas mice treated with isotype-matched irrelevant mAb had I gE levels comparable to that of untreated, immunized mice. Subsequent antigen challenges with DNP4-OVA, either at weekly or monthly interval s, failed to evoke an IgE response for greater than 2 months in mice t reated with anti-IgE during the primary sensitization, even though the terminal half-life of the anti-IgE antibody was 7 days. This inhibiti on was specific for DNP4-OVB since the DNP4-OVA-suppressed mice were a ble to respond to keyhole limpet haemocyanin (KLH). To investigate the effects of antibody treatment at the cellular level, passive transfer experiments were performed. The primary DNP-specific IgE response of adoptive transfer recipient mice was the same whether the donor cells were from mice treated with IgG or anti-IgE. Transfer of enriched T- o r B-cell populations indicated that T-cell help was not compromised by administration of the anti-IgE mAb. However, splenocytes from the ant i-IgE-treated mice failed to synthesize IgE in vitro, and how cytometr ic analysis of B cells from anti-IgE-treated mice showed a dose-depend ent decrease in CD23(+) cells following antibody treatment, which corr elated with decreased serum IgE levels. Taken together, the results of these studies suggest that anti-IgE treatment suppresses IgE response s via effects on B cells rather than T cells, possibly through effects on CD23-dependent pathways.