Abstract
Gene knock-out and knock-in mice are becoming increasingly indispensable for mechanism-oriented studies of EAE. Most gene-modified mice are on the C57BL/6 background, for which presently there are only two EAE models available, the MOG peptide 35-55 and the PLP 178-191 peptide induced disease. However, because MS is not a single pathogenic entity, different EAE models are required to reproduce and study its various features. Here we are introducing MBP-PLP fusion protein (MP4)-induced EAE for C57BL/6 mice. B cell- and CD8+ T cell-dependence, as well as multi-determinant recognition are among the unique features of this demyelinating EAE.
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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B-Lymphocytes / drug effects
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B-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / drug effects
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CD8-Positive T-Lymphocytes / immunology
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Disease Models, Animal*
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Encephalomyelitis, Autoimmune, Experimental / chemically induced*
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Encephalomyelitis, Autoimmune, Experimental / genetics
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Genetic Predisposition to Disease / genetics
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Lymphocyte Activation / drug effects
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Lymphocyte Activation / immunology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myelin Basic Protein* / genetics
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Myelin Basic Protein* / immunology
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Myelin Proteolipid Protein* / genetics
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Myelin Proteolipid Protein* / immunology
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Recombinant Fusion Proteins*
Substances
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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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Recombinant Fusion Proteins