小胶质细胞
吞噬作用
淀粉样蛋白(真菌学)
抗体
BETA(编程语言)
β淀粉样蛋白
纤维
淀粉样纤维
免疫球蛋白G
化学
免疫学
神经科学
生物
医学
病理
淀粉样β
生物化学
肽
计算机科学
炎症
疾病
程序设计语言
作者
Yiming Zheng,Yue Zhong,Shoujun Yu,Ruixue Sun,Zhenwei Zhang,Xiaoyan Du,Simon Ming‐Yuen Lee,Zhitong Chen,Weiming Tian,Yuxiao Lai,Bing Song,Yiming Zheng,Zhen Xu
标识
DOI:10.4103/nrr.nrr-d-23-01942
摘要
The peripheral immune system has emerged as a regulator of neurodegenerative diseases such as Alzheimer's disease. Microglia are resident immune cells in the brain that may orchestrate communication between the central nervous system and peripheral immune system, though the mechanisms are unclear. Here, we found that gamma-type immunoglobulin, a product originating from peripheral blood B cells, localized in the brain parenchyma of multiple mouse models with amyloid pathology, and was enriched on microglia but not on other brain cell types. Further experiments showed that gamma-type immunoglobulin bound to microglial cell membranes and led to diverse transcriptomic changes, including upregulation of pathways related to phagocytosis and immunity. Functional assays demonstrated that gamma-type immunoglobulin enhanced microglial phagocytic capacity for amyloid-beta fibrils via its Fc, but not Fab, fragment. Our data indicate that microglia, when exposed to gamma-type immunoglobulin, exhibit an enhanced capacity for clearing amyloid-beta fibrils, potentially via the gamma-type immunoglobulin Fc fragment signaling pathway. This suggests that parenchymal gamma-type immunoglobulin should be further investigated to determine whether it may play a beneficial role against Alzheimer's disease by enhancing microglial function.
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