Th17 cell enhances CD8 T-cell cytotoxicity via IL-21 production in emphysema mice.
Th17 cell enhances CD8 T-cell cytotoxicity via IL-21 production in emphysema mice.
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DOI：
10.1155/2012/898053
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发表时间：
2012
影响因子：
4.6
通讯作者：
Tang HJ
中科院分区：
文献类型：
--
作者：
Duan MC;Huang Y;Zhong XN;Tang HJ
肺气肿是一种主要由吸烟引起的t细胞介导的自身免疫性疾病。Th17细胞和相关细胞因子可能导致这种疾病。然而，Th17细胞在调节肺气肿炎症反应中的可能作用仍有待阐明。本研究通过检测香烟烟雾暴露小鼠和空气暴露小鼠外周血和肺组织中IL-17和IL-21的蛋白水平，分析小鼠外周血和肺组织中CD4+IL-17+(Th17)细胞、IL-21+Th17细胞和CD8+IL-21R+ T细胞的频率及其与肺气肿病变的关系，探讨IL-21对体外细胞毒性CD8+ T细胞功能的影响。结果发现，cs暴露小鼠的Th17、IL-21+Th17、CD8+IL-21R+ T细胞频率及IL-17、IL-21水平均显著高于空气暴露小鼠，且与肺气肿病变相关。此外，IL-21+Th17细胞的数量与CD8+IL-21R+ T细胞的数量呈正相关。体外实验表明，IL-21显著增强了cs暴露小鼠CD8+ T细胞穿孔素和颗粒酶B的分泌。这些数据间接提供了Th17细胞可能通过调节CD8+细胞毒性t细胞功能参与控制肺气肿局部和系统炎症反应的证据。
Emphysema is a T-cell mediated autoimmune disease caused predominantly by cigarette smoking. Th17 cells and related cytokines may contribute to this disorder. However, the possible implication of Th17 cells in regulating inflammatory response in emphysema remains to be elucidated. In the current study, we tested the protein levels of IL-17 and IL-21 in peripheral blood and lung tissues from cigarette-smoke- (CS-) exposed mice and air-exposed mice, analyzed the frequencies of CD4+IL-17+(Th17) cells, IL-21+Th17 cells, and CD8+IL-21R+ T cells in peripheral blood and lung tissues of mice, and their relationship with emphysematous lesions, and explored the impact of IL-21 on cytotoxic CD8+ T cells function in vitro. It was found that the frequencies of Th17, IL-21+Th17, and CD8+IL-21R+ T cells and the levels of IL-17 and IL-21 of CS-exposed mice were much higher than those of the air-exposed mice and correlated with emphysematous lesions. Additionally, the number of IL-21+Th17 cells positively correlated with the number of CD8+IL-21R+ T cells. The in vitro experiments showed that IL-21 significantly augmented the secretion of perforin and granzyme B in CD8+ T cells from CS-exposed mice. These data indirectly provide evidence that Th17 cells could be involved in the control of the local and system inflammatory response in emphysema by regulating CD8+ cytotoxic T-cell function.
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