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  • 标题:Regulatory T cells percentage in peripheral blood before and after eradication of Helicobacter pylori
  • 本地全文:下载
  • 作者:Yuka Satoh ; Hatsue Ogawara ; Osamu Kawamura
  • 期刊名称:Health
  • 印刷版ISSN:1949-4998
  • 电子版ISSN:1949-5005
  • 出版年度:2014
  • 卷号:06
  • 期号:04
  • 页码:236-242
  • DOI:10.4236/health.2014.64035
  • 语种:English
  • 出版社:Scientific Research Publishing
  • 摘要:Helicobacter pylori (H. pylori) induces gastroduodenal diseases and vigorous humural and cellular immune abnormalities. In order to clarify the immunological changes before and after eradication of H. pylori, the percentages and ratios of the following cells in the peripheral blood of 32 H. pylori-infected patients and 25 control subjects were analyzed: CD4+ T cells, CD8+ T cells, T helper 1 cells (Th1), T helper 2 cells (Th2), CD4+CD25+ T cells, Foxp3+ regulatory T cells (Treg), CD4/CD8 ratio, and Th1/Th2 ratio. CD4/CD8 ratio was significantly higher in H. pylori-infected patients before (mean ± SD, 2.9 ± 1.9) and after (mean ± SD, 2.8 ± 1.6) eradication of H. pylori than in control subjects (mean ± SD, 2.1 ± 0.9). The percentage of Th2 cells was significantly higher in H. pylori-infected patients (mean ± SD, 2.6 ± 1.1) than in control subjects (mean ± SD, 1.9 ± 1.1; p H. pylori (mean ± SD, 2.3 ± 1.4) was lower than that before eradication. There was no significant difference between control subjects (mean ± SD, 4.1% ± 1.5%) and patients before H. pylori eradication (mean ± SD, 4.5% ± 2.4%) in the percentage of Tregs, but the percentage was significantly higher in patients after H. pylori eradication (mean ± SD, 5.2% ±2.6%) than in control subjects. The function of peripheral induced Tregs was reported to suppress the excessive immune reaction in chronic inflammation. These data suggest that Tregs may proliferate and be activated to suppress the activation of humoral immunity in H. pylori-infected patients, and these changes continue after 3 months or later of successful eradication of H. pylori.
  • 关键词:Helicobacter pylori ; Regulatory T Cell; Th1 Cell; Th2 Cell
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