期刊
NATURE COMMUNICATIONS
卷 13, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-022-33932-3
关键词
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资金
- Ministry of Science and Technology China Brain Initiative [2022ZD0204701, 2022ZD0207200]
- National Natural Science Foundation of China [31922027, 32170958, 32000678, 32000727, 32060199, 82171082, 31871038, 32170955]
- Program of Shanghai Academic/Technology Research Leader [21XD1420400]
- Shanghai Pilot Program for Basic Research [21TQ014]
- Shanghai Municipal Science and Technology Major Project
- Innovative Research Team of High-Level Local University in Shanghai
- Shenzhen Science and Technology Research Program [JCYJ20180507182033219, JCYJ20170818152810899]
- Shanghai Municipal Science and Technology Major Project [2018SHZDZX01]
- ZJ Lab
- Guangdong Basic and Applied Basic Research Foundation [2019A1515110948]
- National Postdoctoral Program for Innovative Talent [BX20190354]
Microglial debris clearance plays a crucial role in maintaining CNS homeostasis, with astrocytes being the main cells responsible for the phagocytosis and degradation of microglial debris.
Microglia are important immune cells in the central nervous system (CNS) that undergo turnover throughout the lifespan. If microglial debris is not removed in a timely manner, accumulated debris may influence CNS function. Clearance of microglial debris is crucial for CNS homeostasis. However, underlying mechanisms remain obscure. We here investigate how dead microglia are removed. We find that although microglia can phagocytose microglial debris in vitro, the territory-dependent competition hinders the microglia-to-microglial debris engulfment in vivo. In contrast, microglial debris is mainly phagocytosed by astrocytes in the brain, facilitated by C4b opsonization. The engulfed microglial fragments are then degraded in astrocytes via RUBICON-dependent LC3-associated phagocytosis (LAP), a form of noncanonical autophagy. Interference with C4b-mediated engulfment and subsequent LAP disrupt the removal and degradation of microglial debris, respectively. Together, we elucidate the cellular and molecular mechanisms of microglial debris removal in mice, extending the knowledge on the maintenance of CNS homeostasis.
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