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      Control of microglial neurotoxicity by the fractalkine receptor.

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          Abstract

          Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three different in vivo models, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections, Cx3cr1-/- mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis, Cx3cr1-/- mice showed more extensive neuronal cell loss than Cx3cr1+ littermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability.

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          Author and article information

          Journal
          Nat Neurosci
          Nature neuroscience
          Springer Science and Business Media LLC
          1097-6256
          1097-6256
          Jul 2006
          : 9
          : 7
          Affiliations
          [1 ] Neuroinflammation Research Center and Department of Neurosciences, Lerner Research Institute, Cleveland, Ohio 44195, USA.
          Article
          nn1715
          10.1038/nn1715
          16732273
          0ffdeb28-9678-471e-a68c-467b1ced5a8d
          History

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