Control of microglial neurotoxicity by the fractalkine receptor
摘要：
Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three differentmodels, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections,mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis,mice showed more extensive neuronal cell loss thanlittermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability.
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关键词：
Central Nervous System Microglia Neurons Cells, Cultured Animals Mice, Inbred C57BL Mice, Transgenic Mice Parkinson Disease Motor Neuron Disease
DOI：
10.1088/0004-6256/139/2/728
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