Abstract
To analyze the role of the Th2 cytokine interleukin-5 (IL-5) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-5 gene-knockout (KO) mice in the C57BL/6 background. IL-5 KO mice had a significantly reduced incidence and severity of EAMG. Despite their increased resistance to EAMG, IL-5 KO mice displayed intact secondary antibody and lymphoproliferative responses to acetylcholine receptor (AChR) after immunization with this molecule. However, the relative resistance of IL-5 KO mice was associated with a reduced primary lymphocyte response to AChR, and reduced C3 levels in muscle extracts compared to those in C57BL/6 mice.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adjuvants, Immunologic / genetics
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Adjuvants, Immunologic / metabolism
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Animals
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Autoantibodies / blood
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Complement C3 / metabolism
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Disease Models, Animal
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Epitopes / immunology
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Interferon-gamma / metabolism
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Interleukin-10 / metabolism
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Interleukin-5 / genetics*
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Interleukin-5 / immunology*
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Interleukin-5 / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Muscle, Skeletal / immunology
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Muscle, Skeletal / metabolism
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Myasthenia Gravis / genetics*
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Myasthenia Gravis / immunology*
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Prognosis
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Receptors, Cholinergic / immunology*
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Severity of Illness Index
Substances
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Adjuvants, Immunologic
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Autoantibodies
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Complement C3
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Epitopes
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Interleukin-5
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Receptors, Cholinergic
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Interleukin-10
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Interferon-gamma