Monospecific anti-GD1b IgG is required to induce rabbit ataxic neuropathy

• Published in: Annals of neurology Vol. 45; no. 3; pp. 400 - 403
• Main Authors: Kusunoki, Susumu, Hitoshi, Seiji, Kaida, Ken-Ichi, Arita, Masanobu, Kanazawa, Ichiro
• Format: Journal Article
• Language: English
• Published: New York John Wiley & Sons, Inc 01.03.1999; Willey-Liss
• Subjects: Animals; Antibodies - immunology; Ataxia - immunology; Biological and medical sciences; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction; Gangliosides - immunology; Immunization; Immunoglobulin G - immunology; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Rabbits; Animal model; Nervous system diseases; Antibody; IgG; Rabbit; Autoimmune disease; Lagomorpha; Peripheral neuropathy; Cerebral disorder; Vertebrata; Specificity; Mammalia; Immunological investigation; Animal; Central nervous system disease; Ataxia; Sensory neuron; Peripheral nerve disease; Neurological disorder; Morphometry
• ISSN: 0364-5134; 1531-8249
• DOI: 10.1002/1531-8249(199903)45:3<400::AID-ANA19>3.0.CO;2-Y

Of 22 rabbits sensitized with GD1b, 12 developed experimental sensory ataxic neuropathy. The affected rabbits had a higher level of serum IgG monospecific to GD1b than the unaffected ones. The GD1b‐positive neuronal cytoplasms of rabbit dorsal root ganglia had larger diameters than the negative ones. IgG antibody monospecific to GD1b may preferentially bind to large primary sensory neurons, causing sensory ataxic neuropathy. Ann Neurol 1999;45:400–403