Experimental induction of myelin changes by anti-MAG antibodies and terminal complement complex.
J Neuropathol Exp Neurol
; 54(1): 96-104, 1995 Jan.
Article
em En
| MEDLINE
| ID: mdl-7529298
We investigated the role of anti-myelin-associated glycoprotein (MAG) IgM and complement (C) in the pathogenesis of myelin alterations occurring in patients with anti-MAG-associated polyneuropathy. For this purpose, we separately studied the effects of anti-MAG antibodies and terminal C complex (TCC) after injection into the rabbit sciatic nerve. The two different local treatments produced identical ultrastructural abnormalities such as intramyelinic edema, myelin vesiculation and, in particular, separation of the major dense lines with the formation of widely spaced myelin, a peculiar feature encountered in human peripheral nerve disorders with circulating anti-myelin monoclonal IgM. In nerves treated with anti-MAG IgM ultrastructural myelin alterations were concurrent with activation of the rabbit's own C to the formation of TCC. Contrary to the immunological and ultrastructural findings obtained in C-sufficient animals, in C6-deficient rabbits injected with anti-MAG IgM no myelin alterations nor C completion were observed. This study identifies anti-MAG IgM as the mediator and the C as the effector of myelin changes observed in the present model and, for extension, in human neuropathies associated with anti-MAG IgM.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Imunoglobulina M
/
Complexo de Ataque à Membrana do Sistema Complemento
/
Anticorpos
/
Proteínas da Mielina
/
Bainha de Mielina
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Neuropathol Exp Neurol
Ano de publicação:
1995
Tipo de documento:
Article
País de afiliação:
Itália
País de publicação:
Reino Unido