Abstract
Human immunodeficiency virus (HIV) encephalitis is a prominent pathology seen in children infected with HIV. Immunohistochemical analyses of pediatric brain tissue showed distinct differences in expression of C-C chemokines and their receptors between children with HIV encephalitis and those with non-CNS-related pathologies. Evidence suggests that soluble factors such as HIV Tat released from HIV-infected cells may have pathogenic effects. Our results show Tat effects on chemokines and their receptors in microglia and astrocytes as well as chemokine autoregulation in these cells. These results provide evidence for the complex interplay of Tat, chemokines, and chemokine receptors in the inflammatory processes of HIV encephalitis and illustrate an important new role for chemokines as autocrine regulators.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adolescent
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Astrocytes / drug effects
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Brain / cytology
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Brain / embryology
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Cells, Cultured
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Chemokine CCL2 / metabolism
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Chemokine CCL4
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Chemokines / metabolism*
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Child
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Child, Preschool
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Female
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Gene Expression Regulation / physiology
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Gene Products, tat / pharmacology
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Homeostasis
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Humans
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Immunohistochemistry
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Infant
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Macrophage Inflammatory Proteins / metabolism
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Male
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Microglia / drug effects
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Neuroglia / metabolism*
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Protein Isoforms / metabolism
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Receptors, CCR2
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Receptors, CCR5 / metabolism
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Receptors, CXCR4 / metabolism
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Receptors, Chemokine / metabolism*
Substances
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CCR2 protein, human
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Chemokine CCL2
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Chemokine CCL4
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Chemokines
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Gene Products, tat
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Macrophage Inflammatory Proteins
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Protein Isoforms
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Receptors, CCR2
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Receptors, CCR5
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Receptors, CXCR4
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Receptors, Chemokine