Dehzad Nina, Bopp Tobias, Reuter Sebastian, Klein Matthias, Martin Helen, Ulges Alexander, Stassen Michael, Schild Hansjörg, Buhl Roland, Schmitt Edgar, Taube Christian
III Medical Department, Johannes Gutenberg University, Mainz, Germany.
J Immunol. 2011 Feb 15;186(4):2238-44. doi: 10.4049/jimmunol.1002027. Epub 2011 Jan 17.
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.
哮喘是一种具有不同炎症表型的综合征。动物模型表明，在致敏和过敏原激发后，Th2细胞和Th1细胞会促进过敏性气道疾病的发展。我们之前已经证明，天然存在的调节性T细胞（nTregs）只能轻微抑制Th2诱导的气道炎症和气道高反应性。在本研究中，我们调查了nTreg介导的对Th2诱导和Th1诱导的急性过敏性气道疾病的抑制作用。我们在体内证明，nTregs通过cAMP传递对Th2和Th1诱导的气道疾病发挥其抑制效力。对两种表型的比较显示，尽管cAMP传递相似，但Th1驱动的气道高反应性和炎症对nTreg依赖性抑制更敏感，这表明基于nTreg的潜在治疗策略可能对主要基于Th1反应失调的嗜中性气道炎症患者更有效。
