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Leukocyte and complement activation by GM1-specific antibodies is associated with acute motor axonal neuropathy in rabbits.
van Sorge, Nina M; Yuki, Nobuhiro; Jansen, Marc D; Nishimoto, Yukihiro; Susuki, Keiichiro; Wokke, John H J; van de Winkel, Jan G J; van den Berg, Leonard H; van der Pol, W-Ludo.
Afiliación
  • van Sorge NM; Department of Immunology, University Medical Center Utrecht, Lundlaan 6, 3584 EA Utrecht, The Netherlands.
J Neuroimmunol ; 182(1-2): 116-23, 2007 Jan.
Article en En | MEDLINE | ID: mdl-17161468
Acute motor axonal neuropathy (AMAN) in humans is associated with the presence of GM1-specific antibodies. Immunization of rabbits with GM1-containing ganglioside mixtures, purified GM1, or Campylobacter jejuni lipo-oligosaccharide exhibiting a GM1-like structure elicits GM1-specific antibodies, but axonal polyneuropathy only occurs in a subset of animals. This study aimed to dissect the molecular basis for the variable induction of AMAN in rabbits. Therefore, we analyzed the pro-inflammatory characteristics of GM1-specific antibodies in plasma samples from ganglioside-immunized rabbits with and without neurological deficits. GM1-specific plasma samples from all rabbits with AMAN were capable of activating both complement and leukocytes, in contrast to none of the plasma samples from rabbits without paralysis. Furthermore, GM1-specific IgG-mediated activation of leukocytes was detected before the onset of clinical signs. These data suggest that AMAN only occurs in rabbits that develop GM1-specific antibodies with pro-inflammatory properties.
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Banco de datos: MEDLINE Asunto principal: Autoanticuerpos / Enfermedad de la Neurona Motora / Activación de Complemento / Gangliósido G(M1) / Leucocitos Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: J Neuroimmunol Año: 2007 Tipo del documento: Article País de afiliación: Países Bajos
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Banco de datos: MEDLINE Asunto principal: Autoanticuerpos / Enfermedad de la Neurona Motora / Activación de Complemento / Gangliósido G(M1) / Leucocitos Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: J Neuroimmunol Año: 2007 Tipo del documento: Article País de afiliación: Países Bajos