Control of microglial neurotoxicity by the fractalkine receptor

By A. Cardona, E. Pioro, Margaret E. Sasse, V. Kostenko, Sandra M Cardona, I. Dijkstra, Deren Huang, G. Kidd, S. Dombrowski, Ranjan Dutta and 6 more. Nature Neuroscience, 2006

1,532 citations recorded by the source corpus.

Subfields: Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/c5398cca4c6d5342b3e1568b08deddea57a9ab4f

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Citations in the corpus

Repertoire of microglial and macrophage responses after spinal cord injury (2011, background): “Lack of the fractalkine receptor (CX3CR1) exacerbates neuronal loss in models of Parkinson's disease and amyotrophic lateral sclerosi”
The myeloid cells of the central nervous system parenchyma (2010, background): “The relevance of CX 3 CR1 regulation of microglial-cell activation in vivo was demonstrated by studying toxin-induced neuron injury and genetic models of neurodegeneratio”
Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012, positive): “Microglia were labeled using the CX3CR1+/GFP mouse line in which all microglia express EGFP under the control of fractalkine receptor, CX3CR1, expression (Figure 1 and see Figures S1 and S5 available online; Cardona et al., 2006; Jung et al., 2000; Saederup et al., 2010).”
Microglial cell origin and phenotypes in health and disease (2011, background): “Mice deficient for CX 3 CR1 have a hyperactive microglial cell phenotype and exaggerated neuronal loss in an injury model, a model of Parkinson's disease induced by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and a model of amyotrophic lateral sclerosis (superoxide dismutase 1-transgenic m”
Microglial M1/M2 polarization and metabolic states (2016, background): “state is, in part, due to signals derived from neuronal- and astrocyte-derived factors (Cardona et al., 2006; Neumann et al., 2009; Ransohoff and Cardona, 2010).”
Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging (2010, methodology): “, 2006) or microglial neurotoxicity (Cardona et al., 2006).”
The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “Several mechanisms by which these cells maintain a quiescent state have been proposed, including interaction of microglial CX3CR1 receptor with its neuronal ligand the chemokine CX3CL1 and inhibitory signalling through the microglial cell surface proteins CD172, CD200R and CD45 with their neuronal l”
Macrophages: development and tissue specialization. (2015, background): “Neuronal CX3CL1, CD200, and exosome-derived miR-124 were shown to control microglial cell-autonomous neurotoxicity in various CNS inflammation models (132, 133, 182).”
Heterogeneity of CNS myeloid cells and their roles in neurodegeneration (2011, background): “Study of Alzheimer's disease model mice harboring microglia deficient for the modulatory chemokine receptor CX3CR1 (ref”
Alternatively activated microglia and macrophages in the central nervous system. (2015, methodology): “To further analyze the percentage of microglial cells expressing the markers it is advisable to use immunohistochemistry or flow cytometric analysis (Bedi et al., 2013; Campanella et al., 2002; Cardona et al., 2006a,b; Chiu et al., 2013; Nikodemova and Watters, 2012).”