Eosinophil IgE receptor and CD23

International audienceIn the present review, eosinophil Fc epsilon RII was compared to CD23, a differentiation marker of B cells. Biochemical analysis revealed that molecules of similar molecular weight were immunoprecipitated from eosinophils and B cells by an anti-CD23 monoclonal antibody (mAb) or by BB10, and anti-eosinophil Fc epsilon RII. By flow cytometry, a correlation was found between the binding of anti-CD23 mAb and myeloma IgE. However, a low expression of different epitopes of CD23 was observed in various hypereosinophilic patients. Northern blot analysis of eosinophil RNA with the cDNA probe of CD23 revealed a weak message in only 3 of the 6 patients expressing membrane CD23. The inhibition by anti-CD23 mAbs of IgE-mediated cytotoxicity and IgE binding to eosinophils clearly indicated the participation of CD23 or a related molecule in IgE-dependent eosinophil functions. However, the differential effects of anti-CD23 mAbs on eosinophils and B cells suggest major differences in the characteristics of the molecule expressed by eosinophils and by B cells

Bronchial and nasal responsiveness in atopic asthma and allergic rhinitis patients: Relationship of local responsiveness to cytokine production by peripheral blood mononuclear cells

To investigate the relationship between local responsiveness and allergic symptoms, bronchial and nasal responsiveness were measured in the following four groups of subjects: (i) bronchial asthma patients with serum house dust mite (HDM)-specific IgE antibody; (ii) allergic rhinitis patients with serum HDM-specific IgE antibody; (iii) normal control subjects with HDM-specific IgE antibody; and (iv) normal control subjects without IgE antibody specific for 10 common aero-allergens. Bronchial hyperresponsiveness was detected in all subjects with asthma (group 1) and in some subjects from groups 2 and 3, but not in subjects from group 4. Nasal hyperresponsiveness was found in all subjects with allergic rhinitis (group 2) and in some subjects from groups 1 and 3, but not in subjects from group 4. These findings indicate that local hyperresponsiveness of the non-diseased organ is influenced by an individual's atopic status. Interleukin (IL)-4 and IL-5 production by peripheral blood mononuclear cells (PBMC) was measured after stimulation with HDM in groups 1, 2 and 3 and was found to be similar in all three groups. A correlation between bronchial hyperresponsiveness and in vitro cytokine production was noted in asthma patients. These results suggest that the capacity of IL-4 or IL-5 production by PBMC may reflect local hyperresponsiveness in case of asthma