Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair

Autores
Lopez, Pablo; Zhang, Gang; Zhang, Jiangyang; Lehmann, Helmar C.; Griffin, John W.; Schnaar, Ronald L.; Sheikh, Kazim A.
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
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
Fil: Zhang, Gang. University Johns Hopkins; Estados Unidos
Fil: Zhang, Jiangyang. University Johns Hopkins; Estados Unidos
Fil: Lehmann, Helmar C.. University Johns Hopkins; Estados Unidos
Fil: Griffin, John W.. University Johns Hopkins; Estados Unidos
Fil: Schnaar, Ronald L.. University Johns Hopkins; Estados Unidos
Fil: Sheikh, Kazim A.. University Johns Hopkins; Estados Unidos
Materia
GANGLIOSIDE
GUILLAIN BARRE
ANTI-GANGLIOSIDE ANTIBODIES
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/189118

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network_name_str CONICET Digital (CONICET)
spelling Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repairLopez, PabloZhang, GangZhang, JiangyangLehmann, Helmar C.Griffin, John W.Schnaar, Ronald L.Sheikh, Kazim A.GANGLIOSIDEGUILLAIN BARREANTI-GANGLIOSIDE ANTIBODIEShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Anti-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.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; ArgentinaFil: Zhang, Gang. University Johns Hopkins; Estados UnidosFil: Zhang, Jiangyang. University Johns Hopkins; Estados UnidosFil: Lehmann, Helmar C.. University Johns Hopkins; Estados UnidosFil: Griffin, John W.. University Johns Hopkins; Estados UnidosFil: Schnaar, Ronald L.. University Johns Hopkins; Estados UnidosFil: Sheikh, Kazim A.. University Johns Hopkins; Estados UnidosSociety for Neuroscience2010-07-14info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/189118Lopez, 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; 9533-95410270-64741529-2401CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/30/28/9533.longinfo:eu-repo/semantics/altIdentifier/doi/10.1523/JNEUROSCI.2281-10.2010info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:36Zoai:ri.conicet.gov.ar:11336/189118instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:51:37.144CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
title Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
spellingShingle Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
Lopez, Pablo
GANGLIOSIDE
GUILLAIN BARRE
ANTI-GANGLIOSIDE ANTIBODIES
title_short Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
title_full Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
title_fullStr Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
title_full_unstemmed Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
title_sort Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair
dc.creator.none.fl_str_mv Lopez, Pablo
Zhang, Gang
Zhang, Jiangyang
Lehmann, Helmar C.
Griffin, John W.
Schnaar, Ronald L.
Sheikh, Kazim A.
author Lopez, Pablo
author_facet Lopez, Pablo
Zhang, Gang
Zhang, Jiangyang
Lehmann, Helmar C.
Griffin, John W.
Schnaar, Ronald L.
Sheikh, Kazim A.
author_role author
author2 Zhang, Gang
Zhang, Jiangyang
Lehmann, Helmar C.
Griffin, John W.
Schnaar, Ronald L.
Sheikh, Kazim A.
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv GANGLIOSIDE
GUILLAIN BARRE
ANTI-GANGLIOSIDE ANTIBODIES
topic GANGLIOSIDE
GUILLAIN BARRE
ANTI-GANGLIOSIDE ANTIBODIES
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv 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.
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
Fil: Zhang, Gang. University Johns Hopkins; Estados Unidos
Fil: Zhang, Jiangyang. University Johns Hopkins; Estados Unidos
Fil: Lehmann, Helmar C.. University Johns Hopkins; Estados Unidos
Fil: Griffin, John W.. University Johns Hopkins; Estados Unidos
Fil: Schnaar, Ronald L.. University Johns Hopkins; Estados Unidos
Fil: Sheikh, Kazim A.. University Johns Hopkins; Estados Unidos
description 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.
publishDate 2010
dc.date.none.fl_str_mv 2010-07-14
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/189118
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
0270-6474
1529-2401
CONICET Digital
CONICET
url http://hdl.handle.net/11336/189118
identifier_str_mv 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
0270-6474
1529-2401
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/30/28/9533.long
info:eu-repo/semantics/altIdentifier/doi/10.1523/JNEUROSCI.2281-10.2010
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Society for Neuroscience
publisher.none.fl_str_mv Society for Neuroscience
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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