Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 4, Pages 2238-2244Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002027
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Funding
- Deutsche Forschungsgemeinschaft [TR52 TPA1, SFB 548 A6, TA275/4-1, TA275/5-1]
- International Graduate School of Immunnotherapy [GRK1043 TP C4]
- Carl Zeiss Foundation
- Mainzer Forschungsforderungsprogramm des Fachbereichs Medizin
- Forschungszentrum Immunologie Mainz
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Asthma is a syndrome with different inflammatory phenotypes. Animal models have shown that, after sensitization and allergen challenge, Th2 and Th1 cells contribute to the development of allergic airway disease. We have previously demonstrated that naturally occurring regulatory T cells (nTregs) can only marginally suppress Th2-induced airway inflammation and airway hyperresponsiveness. In this study, we investigated nTreg-mediated suppression of Th2-induced and Th1-induced acute allergic airway disease. We demonstrate in vivo that nTregs exert their suppressive potency via cAMP transfer on Th2- and Th1-induced airway disease. A comparison of both phenotypes revealed that, despite similar cAMP transfers, Th1-driven airway hyperresponsiveness and inflammation are more susceptible to nTreg-dependent suppression, suggesting that potential nTreg-based therapeutic strategies might be more effective in patients with predominantly neutrophilic airway inflammation based on deregulated Th1 response. The Journal of Immunology, 2011, 186: 2238-2244.
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