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dc.contributor.author
Lopez, Pablo
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dc.contributor.author
Zhang, Gang
dc.contributor.author
Zhang, Jiangyang
dc.contributor.author
Lehmann, Helmar C.
dc.contributor.author
Griffin, John W.
dc.contributor.author
Schnaar, Ronald L.
dc.contributor.author
Sheikh, Kazim A.
dc.date.available
2023-02-28T15:50:02Z
dc.date.issued
2010-07-14
dc.identifier.citation
Lopez, Pablo; Zhang, Gang; Zhang, Jiangyang; Lehmann, Helmar C.; Griffin, John W.; et al.; Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair; Society for Neuroscience; Journal of Neuroscience; 30; 28; 14-7-2010; 9533-9541
dc.identifier.issn
0270-6474
dc.identifier.uri
http://hdl.handle.net/11336/189118
dc.description.abstract
Anti-GM1 antibodies are present in some patients with autoimmune neurological disorders. These antibodies are most frequently associated with acute immune neuropathy called Guillain-Barré syndrome (GBS). Some clinical studies associate the presence of these antibodies with poor recovery in GBS. The patients with incomplete recovery have failure of nerve repair, particularly axon regeneration. Our previous work indicates that monoclonal antibodies can inhibit axon regeneration by engaging cell surface gangliosides (Lehmann et al., 2007). We asked whether passive transfer of human anti-GM1 antibodies from patients with GBS modulate axon regeneration in an animal model. Human anti-GM1 antibodies were compared with other GM1 ligands, cholera toxin B subunit and a monoclonal anti-GM1 antibody. Our results show that patient derived anti-GM1 antibodies and cholera toxin β subunit impair axon regeneration/repair after PNS injury in mice. Comparative studies indicated that the antibody/ligand-mediated inhibition of axon regeneration is dependent on antibody/ligand characteristics such as affinity-avidity and fine specificity. These data indicate that circulating immune effectors such as human autoantibodies, which are exogenous to the nervous system, can modulate axon regeneration/nerve repair in autoimmune neurological disorders such as GBS. Copyright © 2010 the authors.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Society for Neuroscience
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
GANGLIOSIDE
dc.subject
GUILLAIN BARRE
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ANTI-GANGLIOSIDE ANTIBODIES
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2023-02-02T23:12:34Z
dc.identifier.eissn
1529-2401
dc.journal.volume
30
dc.journal.number
28
dc.journal.pagination
9533-9541
dc.description.fil
Fil: Lopez, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina
dc.description.fil
Fil: Zhang, Gang. University Johns Hopkins; Estados Unidos
dc.description.fil
Fil: Zhang, Jiangyang. University Johns Hopkins; Estados Unidos
dc.description.fil
Fil: Lehmann, Helmar C.. University Johns Hopkins; Estados Unidos
dc.description.fil
Fil: Griffin, John W.. University Johns Hopkins; Estados Unidos
dc.description.fil
Fil: Schnaar, Ronald L.. University Johns Hopkins; Estados Unidos
dc.description.fil
Fil: Sheikh, Kazim A.. University Johns Hopkins; Estados Unidos
dc.journal.title
Journal of Neuroscience
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/30/28/9533.long
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1523/JNEUROSCI.2281-10.2010
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