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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/189118
Ver los metadatos del registro completo
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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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1842269105777803264 |
score |
13.13397 |