Abstract
Experimental autoimmune myositis (EAM) is a good model of human inflammatory myopathy. We induced EAM in SJL/J mice by injection with myosin and treated inflammatory changes with FK506. The mice developed inflammatory changes after the fifth myosin injection. After treatment with FK506, inflammation was suppressed and central nuclei of the muscle fibers increased. These findings indicate that FK506 is effective in the treatment of EAM. The data suggests that FK506 inhibits interaction with calcineurin. Intercellular adhesion molecule-1 (ICAM-1) positive cells were present in the inflammatory and non-inflammatory areas of EAM. The FK506-treated group stained more weakly for ICAM-1 than the untreated EAM group.
MeSH terms
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Animals
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Cell Nucleus / drug effects
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Cell Nucleus / immunology
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Cell Nucleus / pathology
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Female
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Immunohistochemistry
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Immunosuppressive Agents / pharmacology*
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Intercellular Adhesion Molecule-1 / immunology
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Intercellular Adhesion Molecule-1 / metabolism
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Mice
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Mice, Inbred Strains
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Muscle, Skeletal / drug effects*
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Muscle, Skeletal / immunology
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Muscle, Skeletal / pathology
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Myosins / immunology
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Myosins / pharmacology
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Myositis / drug therapy*
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Myositis / immunology
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Myositis / metabolism
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Nervous System Autoimmune Disease, Experimental / drug therapy*
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Nervous System Autoimmune Disease, Experimental / immunology
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Nervous System Autoimmune Disease, Experimental / metabolism
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Phagocytosis / drug effects
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Phagocytosis / immunology
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Tacrolimus / pharmacology*
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Treatment Outcome
Substances
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Immunosuppressive Agents
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Intercellular Adhesion Molecule-1
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Myosins
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Tacrolimus