TY - JOUR T1 - Circulating IgG autoanti-IgE antibodies in atopic patients block the binding of IgE to its low affinity receptor (CD23) JF - Clinical Molecular Pathology JO - Clin Mol Pathol SP - M342 LP - M346 DO - 10.1136/mp.48.6.M342 VL - 48 IS - 6 AU - S J Smith AU - N S Jones AU - F Shakib Y1 - 1995/12/01 UR - http://mp.bmj.com/content/48/6/M342.abstract N2 - Aims—To investigate the ability of circulating IgG autoanti-IgE antibodies from atopic rhinitis patients to block the binding of IgE to its low affinity receptor (FcεRII), also termed CD23. Methods—This involved the use of a well validated flow cytometric method to detect inhibition of FITC labelled IgE binding to human B cells expressing CD23 (RPMI 8866 cell line). Results—Taking inhibition values greater than 20% as being significant, 15 out of 20 IgG anti-IgE containing sera inhibited the binding of IgE-FITC to the RPMI 8866 cells. The inhibitory effect was recoverable in the IgG fraction of serum, but was not related to the titre of either IgG1 anti-IgE or IgG4 anti-IgE, thus suggesting that it might be related to epitope specificity. No such inhibition was demonstrable with rheumatoid sera containing autoanti-IgG (that is, rheumatoid factor), but lacking autoanti-IgE. Conclusions—The capacity of anti-IgE to block the binding of IgE to CD23 has important implications, particularly in terms of upregulation of IgE synthesis and the consequent perpetuation of the inflammatory response. ER -