Abstract
The aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing-remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA, Copaxone), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ.
Copyright 2010 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Central Nervous System / drug effects
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Central Nervous System / pathology
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Disease Models, Animal
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Encephalomyelitis, Autoimmune, Experimental* / drug therapy
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Encephalomyelitis, Autoimmune, Experimental* / immunology
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Encephalomyelitis, Autoimmune, Experimental* / pathology
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Glatiramer Acetate
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Immunosuppressive Agents / therapeutic use*
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Inflammatory Bowel Diseases / drug therapy
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Inflammatory Bowel Diseases / immunology
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Interleukin-17 / genetics
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Interleukin-17 / metabolism*
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Mice
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Mice, Inbred C57BL
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Multiple Sclerosis, Relapsing-Remitting* / drug therapy
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Multiple Sclerosis, Relapsing-Remitting* / immunology
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Multiple Sclerosis, Relapsing-Remitting* / pathology
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Myelin Proteolipid Protein / immunology
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Peptide Fragments / immunology
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Peptides / therapeutic use*
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Spinal Cord / pathology
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Statistics as Topic
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T-Lymphocytes, Regulatory / drug effects*
Substances
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Immunosuppressive Agents
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Interleukin-17
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Myelin Proteolipid Protein
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Peptide Fragments
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Peptides
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myelin proteolipid protein (139-151)
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Glatiramer Acetate