Abstract
Mechanism-oriented studies of EAE rely mostly on gene-modified mice on the C57BL/6 background. Here we report that MP4-induced EAE displays characteristic differences in CNS pathology as compared to MOG peptide 35-55-elicited disease. While in the latter, the topology of CNS infiltration remained unchanged throughout the disease, in MP4-induced EAE it was dynamic and stage-dependent shifting from the brain to the spinal cord and finally to the cerebellum. Unlike in the MOG peptide model, the frequencies and sizes of CNS lesions in MP4-induced disease showed a clear correlation with clinical disease severity. These characteristic features of MP4-induced EAE may contribute to modelling the complex spectrum of disease manifestations seen in MS.
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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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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Drug Delivery Systems
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Encephalomyelitis, Autoimmune, Experimental / chemically induced*
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Encephalomyelitis, Autoimmune, Experimental / pathology*
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Female
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Glycoproteins / administration & dosage*
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Mice
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Mice, Inbred C57BL
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Myelin Basic Protein / administration & dosage*
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Myelin Proteolipid Protein / administration & dosage*
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments / administration & dosage*
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Recombinant Fusion Proteins / administration & dosage*
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Time Factors
Substances
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Glycoproteins
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MP4 protein, chimeric
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Myelin Basic Protein
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Myelin Proteolipid Protein
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments
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Recombinant Fusion Proteins
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myelin oligodendrocyte glycoprotein (35-55)