Emerging Roles for CSF-1 Receptor and its Ligands in the Nervous System

被引：288

作者：

Chitu, Violeta ^{[1
]}

Gokhan, Solen ^{[2
,3
,4
]}

Nandi, Sayan ^{[5
,6
]}

Mehler, Mark F. ^{[2
,3
,4
]}

Stanley, E. Richard ^{[1
]}

机构：

[1] Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10461 USA

[2] Albert Einstein Coll Med, Inst Brain Disorders & Neural Regenerat, Dept Neurol, Bronx, NY 10461 USA

[3] Albert Einstein Coll Med, Dept Neurosci, Inst Brain Disorders & Neural Regenerat, Bronx, NY 10461 USA

[4] Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Inst Brain Disorders & Neural Regenerat, Bronx, NY 10461 USA

[5] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA

[6] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10461 USA

来源：

TRENDS IN NEUROSCIENCES | 2016年 / 39卷 / 06期

基金：

美国国家卫生研究院;

关键词：

COLONY-STIMULATING FACTOR; HEREDITARY DIFFUSE LEUKOENCEPHALOPATHY; TYROSINE-PHOSPHATASE BETA; ALZHEIMERS-DISEASE; MICROGLIAL PROLIFERATION; CEREBRAL-CORTEX; MOUSE MODEL; SUBVENTRICULAR ZONE; MULTIPLE-SCLEROSIS; CELL-PROLIFERATION;

D O I：

10.1016/j.tins.2016.03.005

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

The colony-stimulating factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and Paneth cell development. However, recent studies in mice have revealed that CSF-1R signaling directly controls the development and maintenance of microglia, and cell autonomously regulates neuronal differentiation and survival. While the CSF-1R-cognate ligands, CSF-1 and interleukin-34 (IL-34) compete for binding to the CSF-1R, they are expressed in a largely non-overlapping manner by mature neurons. The recent identification of a dominantly inherited, adult-onset, progressive dementia associated with inactivating mutations in the CSF-1R highlights the importance of CSF-1R signaling in the brain. We review the roles of the CSF-1R and its ligands in microglial and neural development and function, and their relevance to our understanding of neurodegenerative disease.

引用

页码：378 / 393

页数：16

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