Control of microglial neurotoxicity by the fractalkine receptor - PubMed (original) (raw)

Comparative Study

doi: 10.1038/nn1715. Epub 2006 Jun 18.

Erik P Pioro, Margaret E Sasse, Volodymyr Kostenko, Sandra M Cardona, Ineke M Dijkstra, Deren Huang, Grahame Kidd, Stephen Dombrowski, RanJan Dutta, Jar-Chi Lee, Donald N Cook, Steffen Jung, Sergio A Lira, Dan R Littman, Richard M Ransohoff

Affiliations

• PMID: 16732273
• DOI: 10.1038/nn1715

Comparative Study

Control of microglial neurotoxicity by the fractalkine receptor

Astrid E Cardona et al. Nat Neurosci. 2006 Jul.

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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Comment in

• Fractalkine: moving from chemotaxis to neuroprotection.
  Ré DB, Przedborski S. Ré DB, et al. Nat Neurosci. 2006 Jul;9(7):859-61. doi: 10.1038/nn0706-859. Nat Neurosci. 2006. PMID: 16801915 No abstract available.

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