Abstract
Neurological deficit in experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis is widely considered to be a consequence of synergistic T and B cell responses to central nervous system (CNS) antigens. We show that mice immunized with encephalitogenic myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide develop significant serum levels of anti-MOG antibodies in parallel with disease progression. Furthermore, EAE mice developed antibodies against DNA and RNA, a serological hallmark observed in autoimmune diseases such as systemic lupus erythematosus. The presence of anti-nucleic responsive B cells and antibodies during EAE may highlight a previously unappreciated mechanism in the pathogenesis of CNS autoimmunity.
Copyright © 2011 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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Antibodies, Antinuclear / biosynthesis*
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Antibodies, Antinuclear / blood
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Antibody Specificity
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Autoantibodies / biosynthesis*
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Autoantibodies / blood
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B-Lymphocyte Subsets / immunology
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B-Lymphocyte Subsets / metabolism
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DNA / immunology
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Disease Progression
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / metabolism
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Female
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Glycoproteins / administration & dosage*
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Glycoproteins / immunology*
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Lymphocyte Activation / immunology
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Mice
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Mice, Inbred C57BL
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments / administration & dosage*
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Peptide Fragments / immunology*
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RNA / immunology
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Time Factors
Substances
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Antibodies, Antinuclear
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Autoantibodies
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Glycoproteins
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments
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myelin oligodendrocyte glycoprotein (35-55)
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RNA
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DNA