CD23 DEFICIENT MICE DEVELOP ALLERGIC AIRWAY HYPERRESPONSIVENESS FOLLOWING SENSITIZATION WITH OVALBUMIN

The low affinity receptor for IgE (CD23) is reported to regulate immun e and inflammatory events and as a result, it may have a role in the d evelopment of allergic airway inflammation and hyperresponsiveness (AH R). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensiti zed either intraperitoneally with ovalbumin (OA)/alum or via the airwa ys (10 days exposure to OA aerosol with no adjuvant). Passive sensitiz ation was performed by intravenous injections of OA-specific IgE. Airw ay responsiveness, serum IgE and IgG levels were assessed together wit h airway inflammation. Passive sensitization followed by airway challe nges resulted in increased OA-specific IgG and IgE in the serum of wil d-type mice only, while both the CD23(+/+) and CD23(-/-) groups develo ped tracheal smooth muscle hyperresponsiveness to electrical field sti mulation, indicating that IgE/CD23-mediated immune functions may not b e necessary for the development of allergic changes. Active sensitizat ion of both CD23(-/-) and CD23(+/+) mice resulted in increased serum l evels of OA-specific IgE and IgG, airway eosinophilia and significant AHR when compared with nonsensitized mice. The genetic deficiency of C D23(-/-) mice not only failed to prevent but was associated with a sig nificant increase of these responses. These results indicate that CD23 may not be essential for the development of allergen-induced AHR and further, that its presence may have some inhibitory effects on the all ergic response.