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Chemokine-induced cell death in CCR5-expressing neuroblastoma cells
|Published in||Journal of Neuroimmunology. 2003, vol. 145, no. 1-2, p. 27-39|
|Abstract||CCR5 is expressed in neurons but its function in this cellular context is hitherto poorly understood. We have generated CCR5-expressing SH-SY5Y neuroblastoma cells. CCR5 ligands induced cell death in these cells, but not in control neuroblastoma cells or in CCR5-expressing fibroblasts. CCR5-dependent killing of neuroblastoma cells occurred through apoptosis, since it was accompanied by caspase-3 activation and could be prevented by a caspase-3 inhibitor. Finally, cell killing by activated microglia was more rapid and extensive in CCR5-expressing neuroblastoma cells than in control cells. In summary, CCR5 may act as a death receptor in cells of neuronal lineage and therefore be involved in inflammatory neurodegeneration.|
|Keywords||Animals — Apoptosis/ immunology — Caspase 3 — Caspases/metabolism — Cell Culture Techniques/methods — Cell Death/immunology — Cell Line, Tumor — Chemokines, CC/metabolism/ physiology/ toxicity — Coculture Techniques — Enzyme Activation/immunology — Genetic Vectors — Humans — Ligands — Mice — Microglia/immunology/metabolism — NIH 3T3 Cells — Neuroblastoma/enzymology/ immunology/ pathology — Neurons/enzymology/immunology/pathology — Phagocytosis/immunology — Receptors, CCR5/ biosynthesis/genetics/physiology — Transfection|