首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >The C5a complement activation peptide increases IL-1beta and IL-6 release from amyloid-beta primed human monocytes: implications for Alzheimer's disease.
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The C5a complement activation peptide increases IL-1beta and IL-6 release from amyloid-beta primed human monocytes: implications for Alzheimer's disease.

机译:C5a补体激活肽增加了淀粉样β-引发的人单核细胞的IL-1beta和IL-6释放:对阿尔茨海默氏病的影响。

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摘要

Alzheimer's disease (AD) brains contain large numbers of amyloid-beta peptide (Abeta) deposits associated with activated microglia, astrocytes and dystrophic neurites. Activated complement components and pro-inflammatory cytokines are also present, indicative of focal inflammation. However, neither Abeta, nor the chemokine-like mediator, C5a, which is generated by Abeta-mediated complement activation, significantly activates microglia, as assessed by pro-inflammatory cytokine release. We evaluated the possibility that both together would co-stimulate such release using the THP-1 human monocytic cell line as a microglial surrogate, and found this to be the case. These studies support the hypothesis that Abeta and C5a induce a chronic microglia-mediated focal inflammatory response in AD.
机译:阿尔茨海默氏病(AD)脑包含大量与活化小胶质细胞,星形胶质细胞和营养不良性神经突相关的淀粉样β肽(Abeta)沉积物。还存在活化的补体成分和促炎细胞因子,表明局灶性炎症。但是,由Abeta介导的补体激活产生的Abeta或趋化因子样介质C5a均未激活小胶质细胞,如促炎性细胞因子释放所评估的那样。我们评估了两者一起使用THP-1人单核细胞系作为小胶质细胞替代物共同刺激这种释放的可能性,并发现情况确实如此。这些研究支持Abeta和C5a在AD中诱导慢性小胶质细胞介导的局灶性炎症反应的假说。

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