Neuroprotective role of IL-4 against activated microglia.
Neuroprotective role of IL-4 against activated microglia.
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DOI：
10.4049/jimmunol.151.3.1473
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发表时间：
1993-08
影响因子：
4.4
通讯作者：
C. Chao;T. Molitor;Shuxian Hu
中科院分区：
文献类型：
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作者：
C. Chao;T. Molitor;Shuxian Hu
小胶质细胞已被提出在免疫介导的神经退行性疾病中发挥致病作用。在我们的研究中，使用IFN-γ引发的小胶质细胞/神经元细胞共培养物，我们发现LPS和TNF-α均通过一氧化氮机制引发神经元细胞损伤（γ-氨基丁酸摄取受损和神经元损失）。用IL-4（一种免疫抑制性细胞因子）预处理细胞共培养物，以剂量依赖性方式防止由活化的小胶质细胞诱导的神经元细胞损伤。研究发现IL-4发挥神经保护作用的机制涉及抑制小胶质细胞的IFN-γ启动，随后减少TNF-α和一氧化氮的产生。
Microglia have been proposed to play a pathogenetic role in immunologically mediated neurodegenerative diseases. In our study, using microglial/neuronal cell cocultures primed with IFN-gamma, we found that both LPS and TNF-alpha triggered neuronal cell injury (impairment of gamma-aminobutyric acid uptake and neuronal loss) via a nitric oxide mechanism. Pretreatment of cell cocultures with IL-4, an immunosuppressive cytokine, prevented, in a dose-dependent manner, neuronal cell injury induced by activated microglia. The mechanism by which IL-4 exerts its neuroprotective effect was found to involve the inhibition of IFN-gamma priming of microglia with a subsequent decrease in the production of TNF-alpha and nitric oxide.