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 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.