Critical role of CD23 in allergen-induced bronchoconstriction in a murine model of allergic asthma

CD23-deficient and anti-CD23 monoclonal antibody-treated mice were used to investigate the role of the low-affinity receptor for IgE (CD23) in allergi c airway inflammation and airway hyperresponsiveness (AHR). While there wer e no significant differences in ovalbumin (OVA) specific IgE titers and tis sue eosinophilia, evaluation of lung function demonstrated that CD23(-/-) m ice showed an increased AHR to methacholine (MCh) when compared to wildtype mice but were completely resistant to the OVA challenge. Anti-CD23 Fab fra gment treatment of wild-type mice did not affect the MCh-induced AHR but si gnificantly reduced the OVA-induced airway constriction. These results impl y a novel role for CD23 in lung inflammation and suggest that anti-CD23 Fab fragment treatment may be of therapeutic use in allergic asthma.