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.
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 ataxicpatients may interact closely with GD1b. IgG antibodies highly specific for GD1b may induce ataxia in Guillain-Barré syndrome.
Authors: Kay N Greenshields; Susan K Halstead; Femke M P Zitman; Simon Rinaldi; Kathryn M Brennan; Colin O'Leary; Luke H Chamberlain; Alistair Easton; Jennifer Roxburgh; John Pediani; Koichi Furukawa; Keiko Furukawa; Carl S Goodyear; Jaap J Plomp; Hugh J Willison Journal: J Clin Invest Date: 2009-02-16 Impact factor: 14.808