Abstract
Epidemiological evidence suggests that pathogens may trigger the development of autoimmune diseases such as multiple sclerosis (MS). Pathogens may trigger disease via molecular mimicry, wherein T cells generated against foreign epitopes are also cross-reactive with self-epitopes. Five pathogen-derived molecular mimics of PLP(139-151) (the immunodominant CD4(+) T cell myelin epitope in SJL mice) were previously identified. This study examines the degree of cross-reactivity between the different mimics, comparing mice primed with mimic peptide in CFA with mice infected with recombinant mimic-expressing viruses. The pattern of in vitro reactivity and ability to induce CNS disease differs between peptide priming and virus infection.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / virology
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Cells, Cultured
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Cross Reactions
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Demyelinating Autoimmune Diseases, CNS / immunology*
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Demyelinating Autoimmune Diseases, CNS / virology*
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Disease Models, Animal
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Dose-Response Relationship, Immunologic
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Female
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Freund's Adjuvant / immunology
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Immunodominant Epitopes / genetics
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Immunodominant Epitopes / immunology*
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Mice
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Molecular Mimicry / immunology*
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Myelin Proteolipid Protein / genetics
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Myelin Proteolipid Protein / immunology*
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Peptide Fragments / genetics
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Peptide Fragments / immunology*
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Time Factors
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Viruses / immunology
Substances
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Immunodominant Epitopes
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Myelin Proteolipid Protein
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Peptide Fragments
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myelin proteolipid protein (139-151)
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Freund's Adjuvant