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Am. J. Respir. Crit. Care Med., Volume 156, Number 6, December 1997, 1945-1955

CD23 Deficient Mice Develop Allergic Airway Hyperresponsiveness Following Sensitization with Ovalbumin

ANGELA HACZKU, KATSUYUKI TAKEDA, ECKARD HAMELMANN, AKIHIRO OSHIBA, JOAN LOADER, ANTHONY JOETHAM, CHARLES IRVIN, HITOSHI KIKUTANI, and ERWIN W. GELFAND

Division of Basic Sciences, Department of Pediatrics and Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and Institute for Molecular and Cellular Biology, Osaka University, Suita, Osaka, Japan

The low affinity receptor for IgE (CD23) is reported to regulate immune and inflammatory events and as a result, it may have a role in the development of allergic airway inflammation and hyperresponsiveness (AHR). To test this hypothesis CD23-deficient mice were studied following different modes of allergic sensitization. Mice were actively sensitized either intraperitoneally with ovalbumin (OA)/alum or via the airways (10 days exposure to OA aerosol with no adjuvant). Passive sensitization was performed by intravenous injections of OA-specific IgE. Airway responsiveness, serum IgE and IgG levels were assessed together with airway inflammation. Passive sensitization followed by airway challenges resulted in increased OA-specific IgG and IgE in the serum of wild-type mice only, while both the CD23+/+ and CD23-/- groups developed tracheal smooth muscle hyperresponsiveness to electrical field stimulation, indicating that IgE/CD23-mediated immune functions may not be necessary for the development of allergic changes. Active sensitization of both CD23-/- and CD23+/+ mice resulted in increased serum levels of OA-specific IgE and IgG, airway eosinophilia and significant AHR when compared with nonsensitized mice. The genetic deficiency of CD23-/- mice not only failed to prevent but was associated with a significant 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 allergic response.




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