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CD23 deficient mice develop allergic airway hyperresponsiveness following sensitization with ovalbumin
A Haczku1, K Takeda, E Hamelmann
1Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.
American Journal of Respiratory and Critical Care Medicine
|December 31, 1997
Summary
The low affinity receptor for IgE (CD23) does not appear essential for developing allergic airway hyperresponsiveness (AHR). CD23 deficiency was associated with increased allergic responses, suggesting CD23 may inhibit inflammation.
Area of Science:
- Immunology
- Allergy Research
- Respiratory Medicine
Background:
- The low affinity receptor for IgE (CD23) plays a role in immune regulation.
- Its involvement in allergic airway inflammation and hyperresponsiveness (AHR) is under investigation.
Purpose of the Study:
- To investigate the role of CD23 in the development of allergic airway inflammation and hyperresponsiveness (AHR).
- To determine if CD23-deficient mice exhibit altered responses to allergic sensitization.
Main Methods:
- Studied CD23-deficient (CD23-/-) and wild-type (CD23+/+) mice.
- Utilized active sensitization (ovalbumin/alum or aerosol) and passive sensitization (IgE transfer).
- Assessed airway responsiveness, serum IgE/IgG levels, and airway inflammation.
Main Results:
- Passive sensitization showed IgE/CD23-mediated functions were not necessary for AHR.
- Active sensitization in CD23-/- mice led to increased IgE, IgG, eosinophilia, and AHR compared to controls.
- CD23 deficiency did not prevent allergic responses; it was associated with enhanced allergic reactions.
Conclusions:
- CD23 is not essential for the development of allergen-induced AHR.
- CD23 may possess inhibitory effects on allergic responses.
- Further research into CD23's regulatory role in allergic airway inflammation is warranted.