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Titolo:
EXPERIMENTAL INDUCTION OF MYELIN CHANGES BY ANTI-MAG ANTIBODIES AND TERMINAL COMPLEMENT COMPLEX
Autore:
MONACO S; FERRARI S; BONETTI B; MORETTO G; KIRSHFINK M; NARDELLI E; NOBILEORAZIO E; ZANUSSO G; RIZZUTO N; TEDESCO F;
Indirizzi:
UNIV PADUA,INST NEUROL,VIA GIUSTINIANI 5 I-35138 PADUA ITALY UNIV VERONA,DIPARTIMENTO SCI NEUROL & VIS I-37100 VERONA ITALY UNIV HEIDELBERG,INST IMMUNOL W-6900 HEIDELBERG GERMANY UNIV MILAN,CTR DINO FERRARI,NEUROL INST MILAN ITALY UNIV TRIESTE,INST PATHOL TRIESTE ITALY
Titolo Testata:
Journal of neuropathology and experimental neurology
fascicolo: 1, volume: 54, anno: 1995,
pagine: 96 - 104
SICI:
0022-3069(1995)54:1<96:EIOMCB>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCOPROTEIN ANTIBODIES; PERIPHERAL NEUROPATHY; MONOCLONAL GAMMOPATHY; IGM; DEMYELINATION; RABBITS;
Keywords:
C6-DEFICIENT RABBITS; INTRAMYELINIC EDEMA; MYELIN-ASSOCIATED GLYCOPROTEIN; TERMINAL COMPLEMENT COMPLEX; WIDELY SPACED MYELIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
17
Recensione:
Indirizzi per estratti:
Citazione:
S. Monaco et al., "EXPERIMENTAL INDUCTION OF MYELIN CHANGES BY ANTI-MAG ANTIBODIES AND TERMINAL COMPLEMENT COMPLEX", Journal of neuropathology and experimental neurology, 54(1), 1995, pp. 96-104

Abstract

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, inparticular, separation of the major dense lines with the formation ofwidely 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 wereconcurrent 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, inhuman neuropathies associated with anti-MAG IgM.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 05:27:38