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Titolo:
Anti-GQ1b ganglioside antibodies mediate complement-dependent destruction of the motor nerve terminal
Autore:
OHanlon, GM; Plomp, JJ; Chakrabarti, M; Morrison, I; Wagner, ER; Goodyear, CS; Yin, XH; Trapp, BDT; Conner, J; Molenaar, PC; Stewart, S; Rowan, EG; Willison, HJ;
Indirizzi:
So Gen Hosp, Inst Neurol Sci, Univ Dept Neurol, Glasgow G51 4TF, Lanark, Scotland So Gen Hosp Glasgow Lanark Scotland G51 4TF gow G51 4TF, Lanark, Scotland Glasgow Caledonian Univ, Dept Biol Sci, Glasgow G4 0BA, Lanark, Scotland Glasgow Caledonian Univ Glasgow Lanark Scotland G4 0BA , Lanark, Scotland Univ Strathclyde, Dept Physiol & Pharmacol, Glasgow G1 1XW, Lanark, Scotland Univ Strathclyde Glasgow Lanark Scotland G1 1XW G1 1XW, Lanark, Scotland Leiden Univ, Med Ctr, Dept Physiol, NL-2300 RA Leiden, Netherlands Leiden Univ Leiden Netherlands NL-2300 RA NL-2300 RA Leiden, Netherlands Leiden Univ, Med Ctr, Dept Neurol, NL-2300 RA Leiden, Netherlands Leiden Univ Leiden Netherlands NL-2300 RA NL-2300 RA Leiden, Netherlands Cleveland Clin Fdn, Lerner Res Inst, Cleveland, OH 44195 USA Cleveland Clin Fdn Cleveland OH USA 44195 s Inst, Cleveland, OH 44195 USA
Titolo Testata:
BRAIN
, volume: 124, anno: 2001,
parte:, 5
pagine: 893 - 906
SICI:
0006-8950(200105)124:<893:AGAMCD>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
MILLER-FISHER-SYNDROME; CAMPYLOBACTER-JEJUNI LIPOPOLYSACCHARIDES; CROSS-REACTIVE ANTIBODIES; GUILLAIN-BARRE-SYNDROME; MONOCLONAL-ANTIBODIES; NEUROMUSCULAR-JUNCTIONS; NEUROFILAMENT PROTEINS; BETA-BUNGAROTOXIN; IGG ANTIBODY; END-PLATES;
Keywords:
autoantibody; complement; ganglioside; Miller-Fisher syndrome; neuromuscular junction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Willison, HJ So Gen Hosp, Inst Neurol Sci, Univ Dept Neurol, Glasgow G51 4TF, Lanark, Scotland So Gen Hosp Glasgow Lanark Scotland G51 4TF Lanark, Scotland
Citazione:
G.M. O'Hanlon et al., "Anti-GQ1b ganglioside antibodies mediate complement-dependent destruction of the motor nerve terminal", BRAIN, 124, 2001, pp. 893-906

Abstract

Miller-Fisher syndrome is an autoimmune neuropathy characterized by ataxia, areflexia and ophthalmoplegia, and in the majority of cases the presence of high titres of anti-GQ1b ganglioside antibodies, In an ex vivo model, human and mouse anti-GQ1b antibodies have been shown previously to induce a complement-dependent alpha -latrotoxin-like effect on the murine motor endplate, i.e. they bring about massive quantal release of acetylcholine and eventually block neuromuscular transmission, Using immunofluorescence microscopy with image analysis, we show here that the late stages of this electrophysiological effect temporally coincide with the loss of heavy neurofilament(200 kDa) and type III beta -tubulin immunostaining and structural breakdown of the nerve terminal, as demonstrated by electron microscopy. Ultrastructurally, axon terminals were disorganized, depleted of vesicles, and subdivided by the infiltrating processes of capping Schwann cells, These findings provide clear pathological evidence to support a role for anti-ganglioside antibodies in mediating nerve terminal injury and further advance the view that this site may be of importance as a target in some human neuropathies.

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Documento generato il 26/09/20 alle ore 22:22:56