Abstract
To test the feasibility of classical complement pathway manipulation in experimental autoimmune myasthenia gravis (EAMG) treatment, C57BL/6 (B6) and RIIIS/J mice with EAMG were treated with 10 microg or 100 microg of anti-C1q Ab or isotype Ab. Treatment with 10 microg anti-C1q Ab significantly reduced the clinical severity, decreased lymph node cell IL-6 production and T cell populations. Conversely, administration of 100 microg anti-C1q Ab caused harmful side effects such as increased serum anti-acetylcholine receptor antibody, immune complex, C3 and lymph node B cell levels and kidney C3 and IgG deposits, which reduced the treatment efficacy.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies / blood
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Antibodies / pharmacology*
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Antigen-Antibody Complex / blood
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B-Lymphocytes / pathology
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Complement C1q / immunology*
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Complement C3 / metabolism
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Complement System Proteins / metabolism
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Feasibility Studies
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Immunoglobulin G / metabolism
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Interleukin-6 / biosynthesis*
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Kidney / metabolism
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Lymph Nodes / metabolism
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Lymph Nodes / pathology
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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 / metabolism
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Myasthenia Gravis / pathology*
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Myasthenia Gravis / physiopathology*
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Receptors, Cholinergic / immunology
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Severity of Illness Index
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T-Lymphocytes / pathology*
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Torpedo
Substances
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Antibodies
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Antigen-Antibody Complex
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Complement C3
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Immunoglobulin G
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Interleukin-6
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Receptors, Cholinergic
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Complement C1q
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Complement System Proteins