| First Author | Dasic G | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 9 | Pages | 2957-67 |
| PubMed ID | 10508270 | Mgi Jnum | J:57738 |
| Mgi Id | MGI:1345600 | Doi | 10.1002/(SICI)1521-4141(199909)29:09<2957::AID-IMMU2957>3.0.CO;2-4 |
| Citation | Dasic G, et al. (1999) Critical role of CD23 in allergen-induced bronchoconstriction in a murine model of allergic asthma. Eur J Immunol 29(9):2957-67 |
| abstractText | 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. |
