Abstract:
: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.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Dasic G,Juillard P,Graber P,Herren S,Angell T,Knowles R,Bonnefoy JY,Kosco-Vilbois MH,Chvatchko Ydoi
10.1002/(SICI)1521-4141(199909)29:09<2957::AID-IMMkeywords:
subject
Has Abstractpub_date
1999-09-01 00:00:00pages
2957-67issue
9eissn
0014-2980issn
1521-4141journal_volume
29pub_type
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