Abstract
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-1β, IFN-γ, 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.
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