Abstract
Remyelination in multiple sclerosis (MS) occurs spontaneously and extensively. The underlying mechanisms, however, are only partly understood. Findings in experimental animal settings suggest that inflammation promotes remyelination and repair. Here, we characterized the chemokine receptor expression profiles of macrophages/microglia in early remyelinating and completely remyelinated lesions compared with active demyelinating and inactive demyelinated MS lesions obtained in the early disease course. Biopsy material consisting of 16 MS cases was available for this study. We found that macrophages/microglia within early remyelinating lesions expressed predominantly CCR5. Our findings implicate a possible role of CCR5(+) cells in initiating remyelination.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Antigens, CD / metabolism
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Antigens, Differentiation, Myelomonocytic / metabolism
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Biopsy
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Female
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Humans
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Immunohistochemistry
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Macrophages / immunology
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Macrophages / metabolism*
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Male
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Microglia / immunology
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Microglia / metabolism*
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Middle Aged
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Monocytes / immunology
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Monocytes / metabolism
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Multiple Sclerosis, Chronic Progressive / immunology
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Multiple Sclerosis, Chronic Progressive / metabolism*
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Multiple Sclerosis, Chronic Progressive / pathology
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Multiple Sclerosis, Relapsing-Remitting / immunology
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Multiple Sclerosis, Relapsing-Remitting / metabolism*
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Multiple Sclerosis, Relapsing-Remitting / pathology
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Nerve Regeneration / immunology*
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Receptors, CCR5 / metabolism*
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Receptors, CCR7 / metabolism
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Recovery of Function / immunology*
Substances
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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CCR7 protein, human
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CD68 antigen, human
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Receptors, CCR5
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Receptors, CCR7