Peripheral blood lymphocytes of atopic patients were analyzed with regard to spontaneous as well as mitogen-induced CD23 expression, sCD23 release as well as Ig (M, G, A, E) synthesis in vitro. The data were correlated with the results for phenotypically defined peripheral cells (T cells, B cells, monocytes), sCD23 release and amounts of Ig (M, G, A, E). A positive correlation was obtained for serum sCD23 and serum IgE of patients with high and intermediate IgE levels, of sCD23 with the percentage of B cells and sCD23 with serum IgA levels. No correlation was obtained for the mitogen (SAC, PWM) induced amounts of Ig (E, A, M, G) synthesis and, furthermore, sCD23 levels determined in cell culture did not correlate with serum IgE levels. Our data support the role of sCD23 in atopic diseases and in isotype regulation.

factors are discussed as potential diagnostic parameters of atopic disorders. The amounts of sCD23 in sera from newborn children (n = 4,329) were determined by radioimmunoassay with monoclonal antibodies specific for CD23. The sCD23 levels ranged between 0 and 81.5 ng/ml of CD23-specific mAb. Furthermore, the sera of newborns with more than 5 ng/ml (n = 45) were analyzed by SDS/PAGE and subsequent autoradiography using ¹²⁵I-labeled IgE (PS). These experiments indicate that newborn sera with normal sCD23 amounts contain an IgE-binding activity with a molecular weight of 25 kD; this component was not observed within sera containing elevated amounts ( > 5 ng/ml). In addition, a 60-kD IgE-binding component was detected within most of all newborn sera (76.4%). The data show that the IgE-binding pattern of newborn children and the pattern of adult donors are different. Our data suggest that the measurement of quantitative sCD23 amounts combined with the analysis of the molecular weight pattern of the IgE-binding factors might be a helpful diagnostic parameter with regard to IgE-associated diseases.

The low-affinity receptor for IgE (FcεRII, CD23) and the related soluble IgE-binding factors (IgE-BF; sCD23) play an important role in IgE regulation. Sera of patients suffering from atopic dermatitis (AD) were reported to contain an IgE-binding component with a molecular weight of 60 kD. The aim of our studies was the isolation and characterization of the 60 kD component. Sera of patients with AD were fractionated by ammonium sulfate precipitation (10–90%). The fractions were analyzed with regard to their IgE and their IgE-BF contents. Furthermore, sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis and subsequent autoradiography with ¹²⁵I-labeled human IgE (PS) was performed to detect IgE-binding activity. The major amount of IgE as well as IgE-BF was obtained within the 30–50% ammonium sulfate precipitation. In addition, IgE-binding activity was precipitated at 60% saturation. Separation by gel filtration under physiological conditions indicated IgE-BF with molecular weight of > 100, 60, 25 and 15 kD. Rechromatography of the > 100-kD fraction led to IgE-binding activity with a molecular weight of 60 kD which is not present within normal sera. The data demonstrate that the 60-kD component is partially bound to serum IgE. One may suggest that the complex is involved in the induction and persistence of allergic disorders.