中文摘要：

背景： CD4 (+) CD25 (+)规章的 T 细胞( Tregs )调停通过与表面分子的房间房间接触的有免疫力的抑制，特别地细胞毒素的 T 联系淋巴细胞的抗原 4 ( CTLA-4 )， 导致glucocorticoid 的肿瘤坏死因素受体家庭相关的蛋白质( GITR )，和转变生长因素贝它(TGF贝它)，但是很少在气喘的致病对 Tregs 的准确角色被知道。这研究寻求了在外部血上描绘表面标记的表示，并且在他们上调查吸入的皮质甾的效果在有变应性气喘和健康题目的病人的单音的原子导出房间的 Tregs。方法：CD4 (+) CD25 (高度) Tregs 上的表面分子的表示被流动血细胞计数检测。Tregs 上的表面分子的表示上的吸入的皮质甾的效果是坚定的在活体内和在试管内。全部的浆液免疫球蛋白 E (IgE ) 和高敏感的 C 反应的蛋白质被连接的酶测量免疫吸着剂试金和乳胶分别地提高了 immunoturbidimetric 试金。结果：外部 Tregs 的相等的数字与变应性气喘在病人被发现(稳定、尖锐) 并且健康题目。Tregs 优先地表示了 CTLA-4， GITR，像使用费的受体 4 (TLR4 ) ，联系潜伏的肽(LAP/TGF-beta1 ) ，和叉头关 P3 (FOXP3 ) 。有尖锐气喘的病人减少了 CD4 (+) CD25 (高度) 的数字与健康题目和稳定的 asthmatics 相比舔(+) T 房间。吸入的皮质甾提高了 dose-dependently 表示臀部在活体内和在试管内的 Tregs 的百分比。而且，表示臀部的 Tregs 的百分比否定地与全部的浆液 IgE 层次和气喘的严厉被相关，但是断然与气喘在病人在预言的价值的一第二个百分比与强迫的吐气的体积相关。结论：结果建议膜界限 TGF-beta1 是预言气喘的严厉的一个潜在的候选人，并且可以贡献气喘的持续宽恕。他们的表面标记上的策略指向 Tregs，特别 TGF-beta1，为气喘的未来治疗是有希望的。

英文摘要：

Background CD4^＋CD25^＋ regulatory T cells （Tregs） mediate immune suppression through cell-cell contact with surface molecules, particularly cytotoxic T lymphocyte-associated antigen 4 （CTLA-4）, glucocorticoid-induced tumor necrosis factor receptor family-related protein （GITR）, and transforming growth factor β （TGF-β）, but little is known about the exact role of Tregs in the pathogenesis of asthma. This study sought to characterize the expression of surface markers on peripheral blood mononuclear cells-derived Tregs in patients with atopic asthma and healthy subjects, and to investigate the effect of inhaled corticosteroid on them. Methods The expression of surface molecules on CD4^＋CD25^high Tregs was detected by flow cytometry. The effect of inhaled corticosteroid on expression of the surface molecules on Tregs was determined in vivo and in vitro. Total serum immunoglobulin E （IgE） and high-sensitivity C-reactive protein were measured by enzyme linked immunosorbent assay and latex enhanced immunoturbidimetric assay, respectively. Results Equivalent numbers of peripheral Tregs were found in patients with atopic asthma （stable and acute） and healthy subjects. Tregs preferentially expressed CTLA-4, GITR, toll-like receptor 4 （TLR4）, latency-associated peptide （LAP/FGF-β1）, and forkhead box P3 （FOXP3）. Patients with acute asthma had decreased numbers of CD4^＋CD25^highLAP^＋ T cells compared to healthy subjects and stable asthmatics. Inhaled corticosteroid enhanced the percentage of Tregs expressing LAP in vivo and in vitro dose-dependently. Furthermore, the percentages of Tregs expressing LAP were negatively correlated with total serum IgE levels and severity of asthma, but positively correlated with forced expiratory volume in one second percentage of the predicted value in patients with asthma. Conclusions The results suggest that membrane-bound TGF-β1 is a potential candidate for predicting the severity of asthma, and may contribute to the sustained remission