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Demyelination in vivo by Guillain‐Barré Syndrome and other human serum
Author(s) -
Brown Mark J.,
Rosen Janet L.,
Lisak Robert P.
Publication year - 1987
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880100310
Subject(s) - guillain barre syndrome , medicine , in vivo , myelin , immunology , polyneuropathy , axonal degeneration , pathology , demyelinating disease , chronic inflammatory demyelinating polyneuropathy , antibody , multiple sclerosis , central nervous system , biology , microbiology and biotechnology
Serum from patients with acute inflammatory polyneuropathy (the Guillain‐Barré syndrome, GBS) demyelinates peripheral nerves in vivo more intensely than control human serum. To clarify the processes leading to demyelination we injected rat sciatic nerves with serum from GBS and control subjects in the presence of complement and examined the sequential morphologic changes over 7 days. One day after injection, five of six GBS sera but none of seven control sera caused vesicular demyelination; 3–5 days after injection both GBS and control sera produced macrophage‐mediated demyelination. These observations suggest that GBS serum can initiate acute myelin injury through a humoral mechanism that is disease associated. This response appears to be distinct from delayed cell‐mediated serum‐induced demyelination that is not disease specific.