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Science 28 August 1981:
Vol. 213. no. 4511, pp. 1027 - 1030
DOI: 10.1126/science.7268405
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Articles

Science, Vol 213, Issue 4511, 1027-1030
Copyright © 1981 by American Association for the Advancement of Science

articles

Myeloma neuropathy: passive transfer from man to mouse

UA Besinger, KV Toyka, AP Anzil, A Fateh-Mognadam, R Rouscher, and K Heininger

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.


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