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首页> 外文期刊>The European Journal of Neuroscience >Selective ablation of bone marrow-derived dendritic cells increases amyloid plaques in a mouse Alzheimer's disease model.
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Selective ablation of bone marrow-derived dendritic cells increases amyloid plaques in a mouse Alzheimer's disease model.

机译:在小鼠阿尔茨海默氏病模型中,骨髓来源的树突状细胞的选择性消融增加了淀粉样蛋白斑块。

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We have recently shown that the ability of microglia to effectively fight off aggregated beta-amyloid plaque formation and cognitive loss in transgenic mouse models of Alzheimer's disease (Tg-AD), is augmented in response to T-cell-based immunization, using glatiramer acetate (GA). The immunization increases incidence of local CD11c+ dendritic-like cells. It is unclear, however, whether these dendritic cells are derived from resident microglia or from the bone marrow. To determine the origin of this dendritic-cell population, we used chimeric mice whose bone marrow-derived cells express a transgene that allows the cells to be specifically ablated by diphtheria toxin. We show here that T-cell-based immunization of these mice, using GA, induced the recruitment of bone marrow-derived dendritic cells. Depletion of the dendritic cells by systemic injection of diphtheria toxin resulted in significantly increased formation of amyloid plaques. Thus, recruitment of bone marrow-derived dendritic cells evidently plays a role in reducing plaque formation in a mouse model of Alzheimer's disease.
机译:我们最近表明,小胶质细胞有效抵抗阿尔茨海默氏病(Tg-AD)转基因小鼠模型中聚集的β-淀粉样蛋白斑块形成和认知丧失的能力,响应于使用醋酸格拉替雷的基于T细胞的免疫反应(GA)。免疫增加了局部CD11c +树突状细胞的发生率。但是,尚不清楚这些树突状细胞是否来自小胶质细胞或骨髓。为了确定该树突状细胞群的起源,我们使用了嵌合小鼠,其骨髓来源的细胞表达一种转基因,可以使白喉毒素特异性地消融细胞。我们在这里显示使用GA的这些小鼠的基于T细胞的免疫诱导了骨髓来源的树突状细胞的募集。通过全身注射白喉毒素来耗尽树突细胞导致淀粉样斑块的形成显着增加。因此,在早老性痴呆症小鼠模型中,骨髓来源的树突状细胞的募集显然在减少斑块形成中起作用。

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