中国现代神经疾病杂志 ›› 2014, Vol. 14 ›› Issue (6): 526-530. doi: 10.3969/j.issn.1672-6731.2014.06.012

• 临床研究 • 上一篇    下一篇

2 吉兰-巴雷综合征患者外周血Th17细胞和IL-23 表达变化与其发病机制的相关性研究

何改平, 张彬, 张宝文, 乔梁杰   

  1. 300222 天津市第四医院脑系科
  • 出版日期:2014-06-25 发布日期:2014-06-04
  • 通讯作者: 何改平(Email:hgptj@126.com)

A study of the changes of Th17 cells and IL-23 in patients with Guillain-Barré syndrome

HE Gai-ping, ZHANG Bin, ZHANG Bao-wen, QIAO Liang-jie   

  1. Department of Neurology, Tianjin Fourth Hospital, Tianjin 300222, China
  • Online:2014-06-25 Published:2014-06-04
  • Contact: HE Gai-ping (Email: hgptj@126.com)

摘要: 探讨吉兰-巴雷综合征患者外周血Th17 细胞、血清和脑脊液IL-23 表达变化在其免疫发病机制中的作用。流式细胞术和酶联免疫吸附试验显示,吉兰-巴雷综合征组患者外周血Th17 细胞比例[(4.86 ± 0.60)%]和血清IL-23 水平[(111.80 ± 13.84)pg/ml]均高于对照组[(2.71 ± 0.54)%、(72.55 ±8.19)pg/ml],差异有统计学意义(t = 2.616,P = 0.012;t = 2.300,P = 0.026)。吉兰-巴雷综合征组患者经静脉注射免疫球蛋白后,血清和脑脊液IL-23 水平恢复正常[(74.13 ± 6.18)和(72.92 ± 12.09)pg/ml],与治疗前[(110.50 ± 15.66)和(102.30 ± 7.52)pg/ml]相比,差异具有统计学意义(t = 2.557,P = 0.022;t = 1.422,P = 0.046)。吉兰-巴雷综合征患者外周血Th17 细胞比例增加、血清和脑脊液IL-23 水平升高,提示二者可能参与吉兰-巴雷综合征的发生与发展。

关键词: 多发性神经根神经病, T 淋巴细胞, 辅助诱导, 白细胞介素23

Abstract: Guillain- Barré syndrome (GBS) is an acute autoimmune-mediated inflammatory neuropathy. In this paper, the percentage of Th17 in peripheral blood lymphocyte and the level of IL-23 in serum and cerebrospinal fluid (CSF) of patients with GBS were detected. Twenty-five patients with GBS and 20 controls were analyzed. The percentage of Th17 cells in patients with GBS was (4.86 ± 0.60)%, which was higher than that in controls [(2.71 ± 0.54)%; t = 2.616, P = 0.012]. Serum IL-23 increased in patients with GBS [(111.80 ± 13.84) pg/ml vs (72.55 ± 8.19) pg/ml; t = 2.300, P = 0.026]. The level of IL-23 in serum and CSF from patients with GBS before therapy [(110.50 ± 15.66) and (102.30 ± 7.52) pg/ml] declined to normal after therapy [(74.13 ± 6.18) and (72.92 ± 12.09) pg/ml], and the difference was statistically significant (t = 2.557, P = 0.022; t = 1.422, P = 0.046). Th17 cells and IL-23 increased in patients with GBS, indicating that they may involve in the pathogenesis of GBS.

Key words: Polyradiculoneuropathy, T-lymphocytes, helper-inducer, Interleukin-23