Regulatory T cells more effectively suppress Th1-induced airway inflammation compared with Th2.
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.
III Medical Department, Johannes Gutenberg University, Mainz, Germany.
Nina
N
Dehzad
Tobias
T
Bopp
Sebastian
S
Reuter
Matthias
M
Klein
Helen
H
Martin
Alexander
A
Ulges
Michael
M
Stassen
Hansjörg
H
Schild
Roland
R
Buhl
Edgar
E
Schmitt
Christian
C
Taube
D000208:Acute Disease; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D002478:Cells, Cultured; D018920:Coculture Techniques; D004195:Disease Models, Animal; D004198:Disease Susceptibility / Q000276:immunology / Q000473:pathology; D005260:Female; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D008822:Mice, Transgenic; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology* / Q000473:pathology