Hypoxia induces T Helper 17 cell upregulation in cultured peripheral blood mononuclear cells from chronic stage patients of severe cerebral infarction

被引:22
作者
Yin, YanHong [1 ]
Li, GuoZhong [2 ]
机构
[1] Gen Hosp, Chinese People Liberat Army PLA, Dept Neurol, Beijing 100854, Peoples R China
[2] Harbin Med Univ, Clin Med Coll 1, Dept Neurol, Haerbin 150001, Peoples R China
基金
中国国家自然科学基金;
关键词
cerebral infarction; hypoxia; IL-17A; PBMC; Th17; MESSENGER-RNA EXPRESSION; ORGANOTYPIC HIPPOCAMPAL SLICES; OXYGEN-GLUCOSE DEPRIVATION; PROINFLAMMATORY CYTOKINES; RAT; BRAIN; LYMPHOCYTES; STROKE; IL-17; INFLAMMATION;
D O I
10.1111/j.1348-0421.2010.00301.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Studies have shown the IL-17A involvement in human ischemic stroke patients in vivo. Whether the IL-17A expression was originated from Th17 and could be stimulated by hypoxia remained unknown. Here we report the Th17 upregulation in anaerobic cultured PBMC from chronic stage patients of severe cerebral infarction. By using ELISA and FACS we examined IL-1 beta, IFN-gamma, IL-23 and IL-17A protein levels in the supernatants and Th1/Th17 ratios in PBMC. Statistical significance of Th17 but not Th1 upregulation was proved in 6-hr anaerobic cultured patient groups (P < 0.001). Hence, Th17 might be essential in the autoimmune pathogenesis when hypoxia recurs in severe ischemic stroke patients.
引用
收藏
页码:130 / 134
页数:5
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