Abstract
We found a defective suppressor cell function in vitro both in idiopathic chronic inflammatory demyelinating polyneuropathy and in paraproteinemic neuropathy with antibodies to sulfated glucuronyl paragloboside. In the presence of interferon beta, suppressor cell function was normalized. Our results suggest that a decreased suppressor cell function plays a pathogenetic role in dysimmune neuropathies. Interferon beta might represent an adjunctive therapy in CIDP both acting on a defective blood-nerve barrier and normalizing an otherwise defective suppressor cell function.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Adult
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Aged
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Antibodies, Monoclonal / blood
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Child
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Demyelinating Diseases / immunology
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Demyelinating Diseases / therapy*
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Female
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Globosides / immunology
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Humans
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Immunoglobulin M / blood
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Interferon-beta / administration & dosage*
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Male
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Middle Aged
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Myelin-Associated Glycoprotein / immunology
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Paraproteinemias / immunology
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Paraproteinemias / therapy*
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Peripheral Nervous System Diseases / immunology
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Peripheral Nervous System Diseases / therapy*
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Polyneuropathies / immunology
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Polyneuropathies / therapy
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Recombinant Proteins / administration & dosage
Substances
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Antibodies, Monoclonal
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Globosides
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Immunoglobulin M
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Myelin-Associated Glycoprotein
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Recombinant Proteins
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sulfate-3-glucuronyl paragloboside
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Interferon-beta