期刊文献+

IL-13和CD86对9HTE细胞株和哮喘患儿PBMC表达CD86水平的影响 被引量:1

CD86 expression on 9HTE cell line and on PBMC from children with asthma and treated with recombined human IL-13 and anti-CD86 McAb
原文传递
导出
摘要 目的 了解IL -13和CD86在哮喘发病中的作用及anti CD86McAb治疗哮喘的机理。方法 随机选择门诊哮喘急性发作期患儿30例,正常健康儿童30例作为健康对照组。分别用rhIL -13、TNF- α和rhIL- 13+TNF -α干预9HTE人气道上皮细胞株和哮喘患儿外周血单个核细胞(peripheralbloodmononuclearcell,PBMC) ,用直接免疫荧光流式细胞术(FCM)检测9HTE人气道上皮细胞株表达CD86的百分率、PBMC中CD14 + 细胞表达CD86的平均荧光强度(MFI)及脂多糖(LPS)刺激后PBMC中CD19+ CD86 + 双阳性细胞百分率。结果 (1)分别用TNF- α、rhIL- 13和TNF- α+rhIL -13干预9HTE细胞株后CD86的表达,三组之间表达的百分率差异无统计学意义;rhIL- 13+anti- CD86McAb干预9HTE细胞株后,9HTE细胞表达CD86水平较其他组降低,差异有统计学意义。(2 )哮喘组中的空白组、IL- 13组、TNF -α组、TNF- α+IL -13组及anti CD86组的CD14 + CD86 + 的平均荧光强度和CD19+ CD86 + 百分率均较相应的对照组高,差异有统计学意义。(3)TNF -α+IL -13干预后,CD14 + CD86 + 的平均荧光强度和CD19+ CD86 + 百分率较对应的空白组、IL -13组和TNF -α组明显增高,差异有统计学意义;(4)anti CD86McAb干预后,CD14 + CD86 + 的平均荧光强度和CD19+ CD86 + 百分率较对应? Objective To explore the role of IL-13 and CD86 in the pathogenesis of asthma. MethodsThe blood samples were taken from 30 asthma children( including 18 male and 12 female) and 30 normal children (17 male and 13 female). Direct immunofluorescence flow cytometry was used to detect the CD86+ cell percentage in 9HTE cells and mean fluorescence intensity(MFI) on CD14+ cell and CD19+CD86+ cell percentage in PBMC activated by LPS after treatment with rhIL-13,TNF-α,rhIL-13+TNF-α and anti-CD86 McAb respectively. Results(1) 9HTE cell line expressed CD86 when treated with TNF-α,rhIL-13 and rhIL-13+TNF-α respectively, there was no significant difference among three groups; the level of CD86 expression on 9HTE cell line was significantly lower than that of other three groups when treated with rhIL-13+anti-CD86 McAb; (2) The level of mean fluorescence intensity on CD14+CD86+ and level of CD19+CD86+ percentage in blank, IL-13, TNF-α, TNF-α+IL-13 and anti-CD86 McAb groups of asthmatic group were significantly higher than that in control group; (3) The level of mean fluorescence intensity on CD14+CD86+ and level of CD19+CD86+ percentage treated with TNF-α+IL-13 were significantly higher than that of blank,IL-13,TNF-α in asthmatic and control groups respectively; (4) The level of mean fluorescence intensity on CD14+CD86+ and level of CD19+CD86+ percentage treated with anti-CD86 McAb were significantly lower than that of blank,IL-13,TNF-α, TNF-α+IL-13 groups of asthma and control respectively. Conclusion IL-13 was able to induce CD86 expression on 9HTE cell line,CD14+ and CD19+ in PBMC; anti-CD86 McAb could stop CD86 expression on 9HTE cell line, CD14+ and CD19+ in PBMC. The results suggest that IL-13 and CD86 may play an important role in the pathogenesis of asthma.
出处 《中华微生物学和免疫学杂志》 CAS CSCD 北大核心 2005年第4期273-276,共4页 Chinese Journal of Microbiology and Immunology
基金 国家自然科学基金资助项目 (3 0 2 713 80 )
  • 相关文献

参考文献16

  • 1Vogel G. Interleukin-13's key role in asthma shown. Science, 1998, 282: 2168.
  • 2Masha WK, Jackie L, Xueying X, et al. Interleukin-13: central mediator of allergic asthma. Science, 1998, 282(18): 2258-2260.
  • 3Lordan JL, Davies DE, Wilson SJ, et al. The role of CD28-B7 costimulation in allergen-induced cytokine release by bronchial mucosa from patients with moderately severe asthma. J Allergy Clin Immunol, 2001, 108(6): 976-981.
  • 4Balbo P, Silvestri M, Rossi GA, et al. Differential role of CD80 and CD86 on alveolar macrophages in the presentation of allergen to T lymphocytes in asthma. Clin Exp Allergy, 2001, 31(4): 625-636.
  • 5儿童哮喘防治常规(试行)[J].中华儿科杂志,1998,36(12):747-751. 被引量:2372
  • 6Zhu ZR, Homer J, Wang Z, et al. Pulmonary expression of interleukin-13 cause inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. J Clin Invest, 1999, 103: 779-787.
  • 7Marsha WK. IL-12/IL-13 axis in allergic asthma. J Allergy Clin Immunol, 2001, 107: 9-18.
  • 8Grunig G, Warnock M, Wakil AE, et al. Requirement for IL-13 independently of IL-4 in experimental asthma. Science, 1998, 282: 2261-2263.
  • 9Webb DC, Mckenzie AN, Koskinen M, et al. Integrated signals between IL-13, IL-4 and IL-5 regulate airways hyperreactivity. J Immunol, 2000, 165: 108-113.
  • 10Fujisawa T, Kato Y, Atsuta J, et al. Chemokine production by the BASE-2B human bronchial epithelial cells: differential regulation of eotaxin, IL-8, and RANTES by TH2- and TH1-derived cytokines. J Allergy Clin Immunol, 2002, 105: 126-133.

共引文献2371

同被引文献24

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部