The role of Th1/Th2 cytokines played in regulation of specific CD4 + Th1 cell conversion and activation during inflammatory reaction of chronic obstructive pulmonary disease

Th1/Th2细胞因子在慢性阻塞性肺疾病炎症反应中对特异性CD4+Th1细胞转换和活化的调控作用

阅读:5
作者:J Sun, T Liu, Y Yan, K Huo, W Zhang, H Liu, Z Shi

Abstract

CD4 + Th1-CXCR3 signalling pathway may play a key role in chronic obstructive pulmonary disease (COPD). The aim of this study was to explore Th1/Th2 cytokines ratio differences in patients in different stages of COPD and to confirm the hypothesis that elastin exposure might serve as an antigen to initiate the stimulation of CD4 + Th1-CXCR3 immune inflammation pathway. Patients of COPD in different stages and normal individuals were enrolled. Ten millilitres of peripheral blood was drawn from patients. The concentration of CXCR3, IFN-γ, IL-2, IL-4 and IL-13 in plasma was detected by ELISA. The Naïve CD4+ T cells were isolated from the peripheral blood mononuclear cells, which were stimulated by elastin and collagen before determining the level of IFN-γ secretion by ELISPOT. Compared with control group, the concentration of CXCR3 in the acute exacerbation COPD (AECOPD) group was higher (P < .05). The concentration of IFN-γ and IL-2 in AECOPD group was lower than that in remission (P < .05). The concentration of IFN-γ in the AECOPD and remission was higher than that in controls (P < .05), while IL-2 was opposite (P < .01). The concentration of IL-4 and IL-13 in AECOPD group was higher than that in the controls (P < .05). The CD4+ Th1 cells stimulated by the elastin as antigen secreted more IFN-γ than that by collagen (P < .01). CXCR3 was highly expressed in patients with COPD. There were different Th1/Th2 cytokines in different stages of COPD. The CD4+Th1-specific conversion and activation may be an initiator of COPD immune inflammatory response.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。