Abstract
Glioblastoma multiforme (GBM) is the most malignant brain tumor. Microglia/macrophages are found within human GBM where they likely promote tumor progression. We report that CCL5, CCR1, and CCR5 are expressed in glioblastoma. Individual deletion of CCR1 or CCR5 had little to no effect on survival of tumor bearing mice, or numbers of glioblastoma-infiltrated microglia/macrophages or lymphocytes. CCL5 promoted in vitro migration of wild type, CCR1- or CCR5-deficient microglia/macrophages that was blocked by the dual CCR1/CCR5 antagonist, Met-CCL5. These data suggest that CCL5 functions within the glioblastoma microenvironment through CCR1 and CCR5 in a redundant manner.
Copyright © 2012 Elsevier B.V. All rights reserved.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Brain Neoplasms / genetics
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Brain Neoplasms / immunology*
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Brain Neoplasms / pathology
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Cell Movement / immunology*
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Cell Survival / genetics
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Cell Survival / immunology
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Chemokine CCL5 / biosynthesis*
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Chemokine CCL5 / physiology
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Gene Expression Regulation / immunology*
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Glioblastoma / genetics
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Glioblastoma / immunology*
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Glioblastoma / pathology
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Humans
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Macrophages / immunology
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Macrophages / metabolism
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Macrophages / pathology
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Mice
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Microglia / immunology
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Microglia / metabolism
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Microglia / pathology
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Receptors, CCR1 / biosynthesis*
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Receptors, CCR1 / deficiency
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Receptors, CCR1 / genetics
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Receptors, CCR5 / biosynthesis*
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Receptors, CCR5 / deficiency
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Receptors, CCR5 / genetics
Substances
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Ccl5 protein, mouse
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Ccr1 protein, mouse
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Chemokine CCL5
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Receptors, CCR1
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Receptors, CCR5