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Characterization of LPS and interferon-gamma triggered activation-induced cell death in N9 and primary microglial cells: induction of the mitochondrial gateway by nitric oxide.

机译:LPS和干扰素-γ的特征触发了N9和原代小胶质细胞中激活诱导的细胞死亡:一氧化氮诱导线粒体通道。

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摘要

Microglia, the resident immune cells of the central nervous system, are normally quiescent but become activated after infection or injury.1 As activated microglia can promote both damage and protection,1 their numbers require strict regulation, in part by 'activation-induced cell death' (AlCD). In view of the key participation of microglia in neurological disorders,2 knowledge of the molecular mechanism of AlCD is important. Studies have shown that AlCD induced by lipopolysaccharide (LPS) and interferon (FH)y occurs via two pathways, one of them mediated via NO and the other via caspase-11. Many aspects of this process, however, remain to be elucidated. We investigated AlCD induced by LPS and IFNy in mouse N9 microglia5 and rat primary microglia.
机译:小胶质细胞是中枢神经系统的固有免疫细胞,通常处于静止状态,但在感染或受伤后会被激活。1由于激活的小胶质细胞既可以促进损伤也可以促进保护,1其数量需要严格调节,部分原因是“激活诱导的细胞死亡” '(AlCD)。鉴于小胶质细胞在神经系统疾病中的关键参与,2了解AlCD的分子机制非常重要。研究表明,脂多糖(LPS)和干扰素( FH)y诱导的AlCD通过两种途径发生,一种途径是通过NO介导,另一种途径是caspase-11。但是,此过程的许多方面仍有待阐明。我们调查了LPS和IFNγ在小鼠N9小胶质细胞5和大鼠原发性小胶质细胞中诱导的AlCD。

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