Abstract
Immunization with acetylcholine receptor (AChR) causes experimental myasthenia gravis (EMG). The s.c. administration to C57B1/6 mice of synthetic AChR CD4+ epitopes, before and during AChR immunization, reduced the epitope-specific CD4+ responses and the anti-AChR Ab synthesis, and prevented EMG. The s.c. administration of solubilized AChR had effects similar to those of peptide treatment. Sham-tolerized mice had only Th1 anti-AChR cells, whereas peptide-treated mice had also Th2 cells, and Th2-induced anti-peptide Ab. Established EMG was not affected by s.c. peptide treatment, whereas it worsened after s.c. administration of solubilized AChR.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Autoantibodies / biosynthesis
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Autoantibodies / immunology
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CD4-Positive T-Lymphocytes / cytology
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CD4-Positive T-Lymphocytes / immunology
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Cell Division / drug effects
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Cell Division / immunology
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Disease Models, Animal
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Epitopes / immunology*
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Epitopes / pharmacology
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Immune Tolerance / immunology
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Immunization
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Injections, Subcutaneous
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Mice
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Mice, Inbred Strains
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Myasthenia Gravis / immunology*
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Myasthenia Gravis / prevention & control*
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Peptide Fragments / immunology
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Peptide Fragments / pharmacology
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Receptors, Cholinergic / immunology*
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Solubility
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Th2 Cells / immunology
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Torpedo
Substances
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Autoantibodies
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Epitopes
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Peptide Fragments
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Receptors, Cholinergic