Institute of Infection Immunology, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Helmholtz Centre for Infection Research (HZI) Braunschweig and the Hannover Medical School (MHH), Germany.
Eur J Immunol. 2010 Aug;40(8):2259-66. doi: 10.1002/eji.200939972.
Recent studies highlight the role of Treg in preventing unnecessary responses to allergens and maintaining functional immune tolerance in the lung. We investigated the role of Treg during the sensitization phase in a murine model of experimental allergic airway inflammation by selectively depleting the Treg population in vivo. DEpletion of REGulatory T cells (DEREG) mice were depleted of Treg by diphtheria toxin injection. Allergic airway inflammation was induced using OVA as a model allergen. Pathology was assessed by scoring for differential cellular infiltration in bronchoalveolar lavage, IgE and IgG1 levels in serum, cytokine secretion analysis of lymphocytes from lung draining lymph nodes and lung histology. Use of DEREG mice allowed us for the first time to track and specifically deplete both CD25(+) and CD25(-) Foxp3(+) Treg, and to analyze their significance in limiting pathology in allergic airway inflammation. We observed that depletion of Treg during the priming phase of an active immune response led to a dramatic exacerbation of allergic airway inflammation in mice, suggesting an essential role played by Treg in regulating immune responses against allergens as early as the sensitization phase via maintenance of functional tolerance.
最近的研究强调了 Treg 在预防过敏原引起的不必要反应和维持肺部功能免疫耐受中的作用。我们通过体内选择性耗尽 Treg 群，研究了 Treg 在实验性变应性气道炎症的致敏阶段的作用。通过注射白喉毒素来耗尽调节性 T 细胞（DEREG）小鼠的 Treg。使用 OVA 作为模型变应原诱导变应性气道炎症。通过评估支气管肺泡灌洗中的细胞浸润差异、血清中的 IgE 和 IgG1 水平、肺引流淋巴结淋巴细胞的细胞因子分泌分析和肺组织学来评估病理学。使用 DEREG 小鼠使我们首次能够跟踪和专门耗尽 CD25(+) 和 CD25(-) Foxp3(+) Treg，并分析它们在限制变应性气道炎症中的病理中的意义。我们观察到，在主动免疫反应的启动阶段耗尽 Treg 会导致小鼠变应性气道炎症急剧恶化，这表明 Treg 在致敏阶段通过维持功能耐受，早在调节针对过敏原的免疫反应中就发挥了重要作用。
