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

Eur J Immunol. 1999 Sep;29(9):2957-67. doi: 10.1002/(SICI)1521-4141(199909)29:09<2957::AID-IMMU2957>3.0.CO;2-4.


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.

MeSH terms

  • Allergens / immunology*
  • Animals
  • Asthma / immunology*
  • Bronchoconstriction / immunology*
  • Bronchoconstrictor Agents / pharmacology
  • Disease Models, Animal
  • Eosinophils / metabolism
  • Female
  • Immunoglobulin E / biosynthesis
  • Macrophages, Alveolar / metabolism
  • Methacholine Chloride / pharmacology
  • Mice
  • Mice, Congenic
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Ovalbumin / immunology
  • Ovalbumin / metabolism
  • Receptors, Fc / metabolism
  • Receptors, IgE / deficiency
  • Receptors, IgE / metabolism
  • Receptors, IgE / physiology*
  • Time Factors


  • Allergens
  • Bronchoconstrictor Agents
  • Receptors, Fc
  • Receptors, IgE
  • Methacholine Chloride
  • Immunoglobulin E
  • Ovalbumin