Abstract
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.
Original language | English |
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Pages (from-to) | 116-123 |
Number of pages | 8 |
Journal | Journal of Neuroimmunology |
Volume | 182 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - Jan 2007 |
Keywords
- Acute Disease
- Animals
- Autoantibodies
- Axons
- Cell Degranulation
- Complement Activation
- G(M1) Ganglioside
- Immunoglobulin Fab Fragments
- Immunoglobulin G
- Leukocytes
- Motor Neuron Disease
- Muscle Hypotonia
- Paralysis
- Rabbits
- Receptors, IgG
- Journal Article