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Life without microglia
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DOI：10.1016/j.tins.2025.06.006.png)
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Abstract
En 中文
Microglial proliferation, differentiation, and survival are dependent on IL-34 and CSF1, which signal via a common receptor, CSF1R. Mutations in CSF1R in humans and rodents lead to partial or complete microglial deficiency. Experimental models that underpin current views of microglial function and ontogeny may not take sufficient account of differences between inbred mouse strains, as well as species differences. Many neurodevelopmental functions attributed exclusively to microglia are not impaired in congenitally microglia-deficient or microglia-depleted animals. Microglial deficiency is distinct from the effects mutations in microglia-expressed genes that give rise to dysfunctional microglia and neuropathology. Age-dependent pathology in various disease models is accelerated in microglia-deficient animals, suggesting that the nonredundant function of these cells is to protect against neuronal injury.
Keywords:
Csf1r
neural development
myelination
neurodegeneration
synaptic plasticity
neuroinflammation
Journal
IF:
15.1
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