Abstract
Chronic inflammatory demyelinating polyneuropathy (CIDP) is regarded as an autoimmune disorder, but no clearly defined autoimmune mechanism has been described. Although most patients respond to plasma exchange, no convincing role for autoantibodies has yet been demonstrated. In this study, we have successfully passively transferred disease using sera and purified IgG from 4 of 12 patients responsive to plasma exchange by bypassing the blood-nerve barrier by intraneural injection or opening it by activated T cells. The sera from CIDP patients or purified IgG produced marked conduction block and demyelination, but normal sera or IgG or that from patients with multiple sclerosis or other neuropathies did not. These observations strongly support an important role for anti-myelin/Schwann cell autoantibodies in the pathogenesis of CIDP at least in some patients.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials
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Adolescent
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Adoptive Transfer*
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Adult
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Aged
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Animals
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Blood Transfusion
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Complement C3d / analysis
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Demyelinating Diseases / immunology*
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Female
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Fluorescent Antibody Technique, Indirect
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Humans
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Immunoglobulin G / analysis
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Immunoglobulin G / immunology*
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Male
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Middle Aged
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Muscle, Skeletal / physiology
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Muscle, Skeletal / physiopathology
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Neural Conduction / immunology*
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Ovalbumin / immunology
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Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / immunology*
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Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / pathology*
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Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / physiopathology
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Rats
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Rats, Inbred Lew
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Sciatic Nerve / immunology
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Sciatic Nerve / pathology
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Sciatic Nerve / physiopathology
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Transplantation, Heterologous
Substances
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Immunoglobulin G
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Complement C3d
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Ovalbumin