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Allergen provocation increases TH2-cytokines and FOXP3 expression in the asthmatic lung
S Thunberg1, G Gafvelin, M Nord
1Clinical Immunology and Allergy Unit, Department of Medicine, Karolinska Institute, University Hospital, Stockholm, Sweden.
Allergy
|October 23, 2009
Summary
Asthmatic patients show increased regulatory T cells in the lungs after allergen exposure, but still exhibit heightened Th2 cytokine responses. This suggests a potential impairment in suppressing allergic inflammation in the airways.
Area of Science:
- Immunology
- Allergy Research
- Respiratory Medicine
Background:
- Allergic asthma is driven by allergen-specific IgE and T-helper cell type 2 (Th2) responses.
- Investigating local and systemic regulatory mechanisms in early asthmatic responses is crucial.
Purpose of the Study:
- To investigate local and systemic regulatory mechanisms in the early asthmatic response to bronchial allergen provocation.
Main Methods:
- Bronchoalveolar lavage (BAL) and blood sampling in mild asthmatic patients (n=13) and healthy controls (n=14).
- Phenotyping lymphocytes and measuring cytokines in BAL and peripheral blood mononuclear cells (PBMCs) before and after allergen provocation.
- Analyzing PBMC proliferation and cytokine secretion, including effects of CD25(+) cell depletion and IL-10 neutralization.
Main Results:
- Increased CD69(+) and FOXP3(+) lymphocytes in BAL post-allergen provocation in asthmatics.
- Elevated IL-5 levels in BAL fluid of asthmatics compared to controls.
- Allergen-stimulated PBMCs from asthmatics showed increased IL-5 and IL-13 production, unaffected by CD25(+) depletion or IL-10 neutralization.
Conclusions:
- Bronchial allergen provocation increases FOXP3(+) regulatory T cells in asthmatic lungs.
- Despite regulatory cell increase, asthmatics show enhanced Th2 cytokines, suggesting impaired suppression of Th2 responses in the airways.
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