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Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma
Sarah J Ballantyne1, Jillian L Barlow, Helen E Jolin
1Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
The Journal of Allergy and Clinical Immunology
|September 25, 2007
Summary
Interleukin-25 (IL-25) is crucial for developing airway hyperresponsiveness (AHR) in asthma. Neutralizing this cytokine with an antibody offers a potential new therapy for allergic airway inflammation.
Area of Science:
- Immunology
- Respiratory Medicine
- Allergy Research
Background:
- Interleukin-25 (IL-25), a cytokine in the IL-17 family, is involved in type 2 immunity.
- The precise role of IL-25 in antigen-driven airway inflammation and airway hyperresponsiveness (AHR) requires further elucidation.
Purpose of the Study:
- To investigate the potential of a neutralizing antibody against IL-25 as a novel therapeutic strategy for airway inflammation and hyperresponsiveness.
Main Methods:
- Generation of a neutralizing monoclonal antibody (mAb) targeting IL-25.
- Inhibition of IL-25 using the mAb in a mouse model of allergic airway disease.
Main Results:
- Blocking IL-25 effectively prevented AHR in a mouse model of allergic asthma.
- Administration of anti-IL-25 mAb during sensitization reduced IL-5, IL-13, eosinophils, goblet cell hyperplasia, and IgE, preventing AHR.
- Administering anti-IL-25 mAb during the challenge phase also prevented AHR, even with ongoing type 2 inflammation.
Conclusions:
- IL-25 plays a critical role in the development of AHR.
- IL-25 represents a significant therapeutic target for asthma treatment, with potential for blocking human IL-25 activity.
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