Myeloma Neuropathy: Passive Transfer from Man to Mouse

Mice were injected daily, for up to 10 weeks, with purified monoclonal immunoglobulin G from patients with myelomatous polyneuropathy or benign gammopathy. The animals developed a demyelinating polyneuropathy with slowed nerve conduction velocities. The putative antinerve factor may be an antibody s...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1981-08, Vol.213 (4511), p.1027-1030
Main Authors: Besinger, U. A., Toyka, K. V., Anzil, A. P., Fateh-Moghadam, A., Neumeier, D., Rauscher, R., Heininger, K.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Autoimmune Diseases - immunology
Cancer
Cancer research
Demyelinating diseases
Demyelinating Diseases - etiology
Demyelinating Diseases - immunology
Demyelinating Diseases - physiopathology
Female
Humans
Immunization, Passive
Immunoglobulin Fab Fragments
Immunoglobulin Fc Fragments
Immunoglobulin G
Immunoglobulins
Infants
Mice
Multiple Myeloma - complications
Nerves
Nervous system diseases
Neural Conduction
Neurology
Peripheral nervous system diseases
Polyneuropathies
Schwann cells
Sudden infant death syndrome
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Summary:Mice were injected daily, for up to 10 weeks, with purified monoclonal immunoglobulin G from patients with myelomatous polyneuropathy or benign gammopathy. The animals developed a demyelinating polyneuropathy with slowed nerve conduction velocities. The putative antinerve factor may be an antibody since injection of Fab fragments from the monoclonal immunoglobulin G produced a similar demyelination. This provides evidence of a circulating factor in the serum of myeloma patients with polyneuropathy that reproduces typical features of the human disease on passive transfer. This disorder is thus distinguished from other neuropathies that occur as remote effects of malignant disease but have no identified pathogenic factors associated with them.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.7268405