Regulatory T Cells More Effectively Suppress Th1-Induced Airway Inflammation Compared with Th2

被引:27
作者
Dehzad, Nina [1 ]
Bopp, Tobias [2 ]
Reuter, Sebastian [1 ]
Klein, Matthias [2 ]
Martin, Helen [1 ]
Ulges, Alexander [2 ]
Stassen, Michael [2 ]
Schild, Hansjoerg [2 ]
Buhl, Roland [1 ]
Schmitt, Edgar [2 ]
Taube, Christian [1 ]
机构
[1] Johannes Gutenberg Univ Mainz, Dept Med 3, D-55131 Mainz, Germany
[2] Johannes Gutenberg Univ Mainz, Inst Immunol, D-6500 Mainz, Germany
关键词
ALLERGEN-SPECIFIC TH1; MONOCLONAL-ANTIBODY; BRONCHIAL HYPERREACTIVITY; MEDIATED SUPPRESSION; SIGNAL TRANSDUCER; CUTTING EDGE; IFN-GAMMA; TGF-BETA; ASTHMA; HYPERRESPONSIVENESS;
D O I
10.4049/jimmunol.1002027
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:2238 / 2244
页数:7
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