title: GD1b-specific antibody induces ataxia in Guillain-Barre syndrome.
abstract: BACKGROUND
  Rabbit ataxic neuropathy and several case reports have suggested a close association of IgG anti-GD1b antibodies with ataxia in Guillain-Barré syndrome (GBS). However, about half of the patients with GBS having IgG anti-GD1b antibodies with no reactivities against other gangliosides (GD1b-mono IgG) do not exhibit ataxia. Antibodies specific to ganglioside complexes (GSCs) containing GD1b have been found in sera from some patients with GBS.
  
  
  OBJECTIVE
  To investigate whether the reactivities of anti-GD1b IgG to such complexes are different between ataxic and nonataxic patients.
  
  
  METHODS
  The authors examined sera from 17 patients with GBS (9 with ataxia and 8 without ataxia) who had GD1b-mono IgG, with the use of an ELISA in which wells were coated with a mixture of GD1b and each of nine gangliosides (GM1, GM2, GM3, GD1a, GD3, GT1a, GT1b, GQ1b, and GalNAc-GD1a). The binding activities of the anti-GD1b IgG antibodies against such mixture antigens were compared between ataxic and nonataxic patients.
  
  
  RESULTS
  The reactivities to antigens, such as GD1b combined with GD1a, GT1b, GQ1b, and GalNAc-GD1a, were significantly reduced in ataxic compared with nonataxic patients. Sera from all nonataxic patients had antibody activities to GSCs not containing GD1b.
  
  
  CONCLUSIONS
  The addition of another ganglioside may cause conformational change of GD1b. Given the inhibition of the binding ability of the anti-GD1b IgG antibodies by such a conformational change, the anti-GD1b IgG antibodies in ataxic patients may interact closely with GD1b. IgG antibodies highly specific for GD1b may induce ataxia in Guillain-Barré syndrome.
authors.affiliation: Department of Internal Medicine 3, Division of Neurology, National Defense Medical College, Saitama-ken, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kaida
authors.forename: K
authors.initials: K
authors.lastname: Kamakura
authors.forename: G
authors.initials: G
authors.lastname: Ogawa
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: K
authors.initials: K
authors.lastname: Motoyoshi
authors.forename: M
authors.initials: M
authors.lastname: Arita
authors.forename: S
authors.initials: S
authors.lastname: Kusunoki
mesh_terms: D000328:Adult; D000368:Aged; D000915:Antibody Affinity; D000918:Antibody Specificity; D001259:Ataxia / Q000209:etiology* / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis / Q000097:blood / Q000502:physiology*; D001666:Binding Sites, Antibody; D001667:Binding, Competitive / Q000276:immunology; D005260:Female; D005732:Gangliosides / Q000097:blood / Q000737:chemistry / Q000276:immunology*; D020275:Guillain-Barre Syndrome / Q000150:complications* / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011487:Protein Conformation
chemical_list: D001323:Autoantibodies; D005732:Gangliosides; D007074:Immunoglobulin G; C033851:ganglioside, GD1b