期刊
NATURE MEDICINE
卷 22, 期 2, 页码 135-137出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.4022
关键词
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资金
- Advanced European Research Council (ERC) [232835, 309788]
- EU [279017]
- Israeli Science Foundation [1782/11]
- Weizmann-Tanz collaboration for research in Alzheimer's disease
- European Research Council (ERC) [309788] Funding Source: European Research Council (ERC)
Systemic immune suppression may curtail the ability to mount the protective, cell-mediated immune responses that are needed for brain repair. By using mouse models of Alzheimer's disease (AD), we show that immune checkpoint blockade directed against the programmed death-1 (PD-1) pathway evokes an interferon (IFN)-gamma-dependent systemic immune response, which is followed by the recruitment of monocyte-derived macrophages to the brain. When induced in mice with established pathology, this immunological response leads to clearance of cerebral amyloid-beta (A beta) plaques and improved cognitive performance. Repeated treatment sessions were required to maintain a long-lasting beneficial effect on disease pathology. These findings suggest that immune checkpoints may be targeted therapeutically in AD.
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