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[呼吸道合胞病毒毛细支气管炎患儿外周血CD4⁺CD25⁺调节性T细胞和Th17细胞的变化及临床意义]

[Changes and the clinical significance of CD4⁺ CD25⁺ regulatory T cells and Th17 cells in peripheral blood of infants with respiratory syncytial virus bronchiolitis].

作者信息

Li Bin, Wu Fu-Ling, Feng Xue-Bin, Sun Da-Kang, Cui Qing-Qing, Zhao Zhi-Xu

机构信息

Department of Pediatrics, Binzhou Medical University, Binzhou 256603, China.

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2012 Apr;28(4):426-8.

Abstract

AIM

To observe the percentages of CD4(+);CD25(+); regulatory T cells (Tregs) and Th17 cells and the levels of IL-10, TGF-β and IL-17 in peripheral blood of infants with respiratory syncytial virus (RSV) bronchiolitis. The relationship between above cells, cytokines and RSV bronchiolitis was determined.

METHODS

Thirty-three infants with RSV bronchiolitis, twenty-eight infants with non-RSV pneumonia and twenty-six healthy infants were enrolled. The percentages of Tregs and Th17 cells in peripheral blood were detected by flow cytometer (FCM), and the levels of IL-10, TGF-β and IL-17 in plasma were determined by ELISA.

RESULTS

The percentage of Tregs and the levels of IL-10 and TGF-β in infants with RSV bronchiolitis were significantly lower than those in infants with non-RSV pneumonia and healthy infants (P<0.05), while the percentage of Th17 cells and the level of IL-17 in infants with RSV bronchiolitis were significantly higher than those in infants with non-RSV pneumonia and healthy infants (P<0.05).

CONCLUSION

The imbalance between Tregs and Th17 cells in peripheral blood of infants with RSV bronchiolitis may be one of the pathogenesis of RSV bronchiolitis.

摘要

目的

观察呼吸道合胞病毒(RSV)毛细支气管炎患儿外周血中CD4(+)、CD25(+)调节性T细胞(Tregs)和Th17细胞的百分比以及IL-10、TGF-β和IL-17的水平。确定上述细胞、细胞因子与RSV毛细支气管炎之间的关系。

方法

纳入33例RSV毛细支气管炎患儿、28例非RSV肺炎患儿和26例健康婴儿。采用流式细胞仪(FCM)检测外周血中Tregs和Th17细胞的百分比,采用酶联免疫吸附测定(ELISA)法测定血浆中IL-10、TGF-β和IL-17的水平。

结果

RSV毛细支气管炎患儿的Tregs百分比以及IL-10和TGF-β水平显著低于非RSV肺炎患儿和健康婴儿(P<0.05),而RSV毛细支气管炎患儿的Th17细胞百分比和IL-17水平显著高于非RSV肺炎患儿和健康婴儿(P<0.05)。

结论

RSV毛细支气管炎患儿外周血中Tregs和Th17细胞失衡可能是RSV毛细支气管炎发病机制之一。

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