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.
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Authors | G Dasic, P Juillard, P Graber, S Herren, T Angell, R Knowles, J Y Bonnefoy, M H Kosco-Vilbois, Y Chvatchko |
Journal | European journal of immunology
(Eur J Immunol)
Vol. 29
Issue 9
Pg. 2957-67
(09 1999)
ISSN: 0014-2980 [Print] Germany |
PMID | 10508270
(Publication Type: Journal Article)
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Chemical References |
- Allergens
- Bronchoconstrictor Agents
- Receptors, Fc
- Receptors, IgE
- Methacholine Chloride
- Immunoglobulin E
- Ovalbumin
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Topics |
- 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, metabolism)
- Receptors, Fc
(metabolism)
- Receptors, IgE
(deficiency, metabolism, physiology)
- Time Factors
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