期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 216, 期 10, 页码 2265-2281出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20182037
关键词
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资金
- National Institutes of Health [R01CA154947, R01MH104559, U19AI128949, 1RF1 AG054011-01, T32 AG049688, R21MH106919, R01 NS091519]
- Advanced Postdoc Mobility Fellowship of the Swiss National Foundation
- Human Frontier Science Program Organization [LT000110/2015-L/1]
- National Institutes of Health Director New Innovator Award [DP2 MH100012-01]
- Brain and Behavior Research Foundation NARSAD Young Investigator Award [25065]
- National Institute of Mental Health [F30MH111143]
- National Eye Institute [R01EY024918, R01EY 026053, R21EY026702]
- National Institute of Neurological Disorders and Stroke [R21NS105119]
- Naito Foundation
- Uehara Memorial Foundation
- Seaver Foundation
- EMBO Young Investigator Programme award
- National Research Foundation [NFR2016NRF-NRFI001-02]
- Singapore Immunology Network Core Funding
Microglia, the brain resident macrophages, critically shape forebrain neuronal circuits. However, their precise function in the cerebellum is unknown. Here we show that human and mouse cerebellar microglia express a unique molecular program distinct from forebrain microglia. Cerebellar microglial identity was driven by the CSF-1R ligand CSF-1, independently of the alternate CSF-1R ligand, IL-34. Accordingly, CSF-1 depletion from Nestin. cells led to severe depletion and transcriptional alterations of cerebellar microglia, while microglia in the forebrain remained intact. Strikingly, CSF-1 deficiency and alteration of cerebellar microglia were associated with reduced Purkinje cells, altered neuronal function, and defects in motor learning and social novelty interactions. These findings reveal a novel CSF-1-CSF-1R signaling-mediated mechanism that contributes to motor function and social behavior.
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