Inhibition of human interleukin 4‐induced IgE synthesis by a subset of anti‐CD23/FcϵRII monoclonal antibodies

Abstract

Specific monoclonal antibodies (mAb) directed against the CD23 antigen were used to study human interleukin 4 (hIL 4)‐induced IgE production by blood and tonsillar mononuclear cells. Both peripheral blood and tonsillar mononuclear cells stimulated by hIL 4 expressed membrane CD23 as detected by the binding of all anti‐CD23 mAb. Nevertheless, two sets of anti‐CD23 mAb could be distinguished. The first set, including mAb25, was able to decrease significantly hIL 4‐induced IgE synthesis by mononuclear cells. The second set, including EBVCS#1, did not affect hIL 4‐induced IgE synthesis. All the anti‐CD23 mAb were able to bind specifically to a human B cell line expressing recombinant CD23. Inhibition experiments revealed that the two sets of anti‐CD23 mAb did not recognize the same epitope on the CD23 antigen. In fact, all the anti‐CD23 mAb, except EBVCS#1, were able to inhibit IgE binding to CD23 on RPMI 8866 cells. Moreover, the first set of antibodies, which decreased IgE production, was able to up‐regulate membrane CD23 expression on hIL4‐stimulated tonsillar mononuclear cells. Conversely, EBVCS#1, which had no effect on IgE production, did not affect hIL 4‐induced CD23 expression. These results indicate that CD23 plays a key role in human IgE synthesis.