Abstract
Experimental autoimmune encephalomyelitis (EAE), an inflammatory demyelinating disease of the CNS, is regarded as an experimental model for multiple sclerosis. The complement has been implicated in the pathogenesis of multiple sclerosis. To clarify the role of C in mouse EAE, we immunized mice deficient in C3 (C3(-/-)) and their wild-type (C3(+/+)) littermates with myelin oligodendrocyte glycoprotein peptide 35-55. C3(-/-) mice were susceptible to EAE as much as the C3(+/+) mice were. No differences were found for the production of IL-2, IL-4, IL-12, TNF-alpha, and IFN-gamma between C3(+/+) and C3(-/-) mice. This finding shows that C3, a key component in C activation, is not essential in myelin oligodendrocyte glycoprotein peptide-induced EAE in mice.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell-Free System
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Cells, Cultured
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Complement Activation* / genetics
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Complement C3 / biosynthesis
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Complement C3 / deficiency
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Complement C3 / genetics
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Complement C3 / physiology*
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Cytokines / analysis
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Cytokines / metabolism
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Encephalomyelitis, Autoimmune, Experimental / genetics
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Immunohistochemistry
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Injections, Subcutaneous
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Interleukin-12 / analysis
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Interleukin-12 / biosynthesis
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Lymph Nodes / chemistry
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Lymph Nodes / cytology
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Lymph Nodes / immunology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myelin Proteins
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Myelin-Associated Glycoprotein / administration & dosage
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Myelin-Associated Glycoprotein / immunology*
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Myelin-Oligodendrocyte Glycoprotein
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Oligodendroglia / immunology
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Peptide Fragments / administration & dosage
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Peptide Fragments / immunology*
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Spleen / chemistry
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Spleen / cytology
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Spleen / immunology
Substances
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Complement C3
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Cytokines
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Mog protein, mouse
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Myelin Proteins
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Myelin-Associated Glycoprotein
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments
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Interleukin-12