目的：探讨哮喘急性发作期患者外周血中Th17细胞的变化及其与哮喘严重程度的关系。方法：选取轻度急性哮喘患者、重度急性哮喘患者和健康对照者各10名。从血清单个核细胞中分离T淋巴细胞，流式细胞仪检测阳性Th17细胞率，分析其与哮喘严重程度的关系。结果：轻度急性哮喘组和重度急性哮喘组外周血阳性Th17细胞均较健康对照组增高(P＜0.05)，而重度哮喘组高于轻度哮喘组(P＜0.05)。重度哮喘组外周血IL-17水平明显高于轻度哮喘组和健康对照组(P＜0.05)。外周血中Th17阳性细胞数与急性哮喘严重程度呈正相关(r=0.869，P＜0.05)。结论：急性哮喘患者外周血Th17细胞表达增加，且与其病情的严重程度呈正相关。

ObjectiveTo observe the change of peripheral blood Th17 cells and relationship between the severity and Th17 cells in patients with acute asthma.MethodsWe recruited patients with mild acute asthma(n=10) and severe acute asthma(n=10), and healthy volunteers(n=10). T-lymphocytes were collected from the peripheral blood mononuclear cells (PBMC). Flow cytometer (FCM) was used to detect the expression of peripheral blood Th17 cells. IL-17 levels in the peripheral blood were measured by enzyme-linked immunosorbentassay (ELISA).ResultsThe rate of  positive Th17 cells of peripheral blood in the severe acute asthma group was higher than that in the mild acute  asthma group(P＜0.05) and the rate of positive Th17 cells of peripheral blood in healthy volunteer group were the lowest among all groups (P＜0.05, respectively). The level of IL-17 in the peripheral blood of patients with severe acute asthma increased significantly compared with that in patients with mild acute asthma and healthy volunteers (P＜0.05). The positive Th17 cells of peripheral blood in patients with acute asthma were positively correlated with the severity of acute asthma(r=0.869, P＜0.05).ConclusionThe positive rate of Th17 cells in the peripheral blood increases in patients with acute asthma and has positive correlation with the severity of acute asthma.

［1］Hellings P W, Kasran A, Liu Z, et al. Interleukin-17 orchestrates the granulocyte influx into airways after allergen inhalation in a mouse model of allergic asthma［J］. Am J Respir Cell Mol Biol, 2003, 28 (1): 42-50.
［2］Chang S H, Dong C. A novel heterodimeric cytokine consisting of IL-17 and IL-17F regulates inflammatory responses［J］.Cell Res, 2007, 17 (5): 435-440.
［3］张金花,周怡,刘宇. 内源性哮喘免疫支持治疗的探讨［J］.中国现代医学杂志,2007,17(4): 464-465.
ZHANG Jinhua，ZHOU Yi，LIU Yu. Discussion of immutherapy to patients with intrinsic asthma［J］. Chin J Modern Med, 2007, 17(4): 464-465.
［4］Dechene L. Th1/Th2 immune response［J］. J Allergy Clin Immunol, 2002, 110(3): 539-540.
［5］Mckenzie B S, Kasteletin R A, Cua D J, et al. Understanding the IL-23-IL-17 immune pathway ［J］. Trends Immunol, 2006, 27(1):17-23.
［6］Veldhoen M, Hocking R J, Atkins C J, et al. TGF beta in the context of an inflammatory cytokinemilieu supports de novo differentiation of IL-17-producing T cells［J］. Immunity, 2006, 24(2): 179-189.
［7］Weiehler S, Proud D. Interleukin-17A modulates human airway epithelial responses to human rhinovirus infection［J］. Am J Physiol Lung Cell Mol Physiol, 2007, 293(2):505-515.
［8］Zheng Y, Danilenko D M, Valdez P, et al. Interleukin-22, a TH17 cytokine, mediates IL-23 induced dermal inflammation and acanthosis ［J］. Nature, 2007, 445 (7128): 648-651.
［9］Reinhardt R L, Kang S J, Liang H E, et al. T helper cell effector fates-who, how and where?［J］. Curr Opin Immunol, 2006, 18(3): 271-277.
［10］Chung D R, Kasper D L, Panzo R J, et al. CD4+T cells mediate abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism ［J］. J Immunol, 2003, 170(4): 1958-1963.