神经炎症
小胶质细胞
发病机制
免疫系统
免疫学
先天免疫系统
获得性免疫系统
生物
神经科学
炎症
作者
Samuel Marsh,Edsel M. Abud,Anita Lakatos,Alborz Karimzadeh,Stephen T. Yeung,Hayk Davtyan,Gianna Fote,Lydia Lau,Jason G. Weinger,Thomas E. Lane,Matthew A. Inlay,Wayne W. Poon,Mathew Blurton‐Jones
标识
DOI:10.1073/pnas.1525466113
摘要
Significance Neuroinflammation and activation of innate immunity are pathological hallmarks of Alzheimer’s disease (AD). In contrast, very few studies have examined the impact of the adaptive immune system in AD pathogenesis. Here, we find that genetic ablation of peripheral immune cell populations significantly accelerates amyloid pathogenesis, worsens neuroinflammation, and alters microglial activation state. Critically, it appears that loss of IgG-producing B cells impairs microglial phagocytosis, thereby exacerbating amyloid deposition. Conversely, replacement of IgGs via direct injection or bone marrow transplantation reverses these effects and reduces Aβ pathology. Together, these results highlight the importance of the adaptive immune system and its interactions with microglia in the pathogenesis of AD.
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