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- G Dasic, P Juillard, P Graber, S Herren, T Angell, R Knowles, J Y Bonnefoy, M H Kosco-Vilbois, and Y Chvatchko.
- Department of Immunology Geneva Biomedical Research Institute, Glaxo Wellcome Research and Development S.A., Geneva, Switzerland.
- Eur. J. Immunol. 1999 Sep 1; 29 (9): 2957-67.
AbstractCD23-deficient and anti-CD23 monoclonal antibody-treated mice were used to investigate the role of the low-affinity receptor for IgE (CD23) in allergic airway inflammation and airway hyperresponsiveness (AHR). While there were no significant differences in ovalbumin (OVA)-specific IgE titers and tissue eosinophilia, evaluation of lung function demonstrated that CD23-/- mice showed an increased AHR to methacholine (MCh) when compared to wild-type mice but were completely resistant to the OVA challenge. Anti-CD23 Fab fragment treatment of wild-type mice did not affect the MCh-induced AHR but significantly reduced the OVA-induced airway constriction. These results imply a novel role for CD23 in lung inflammation and suggest that anti-CD23 Fab fragment treatment may be of therapeutic use in allergic asthma.
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