POSSIBLE MECHANISM OF INTRAVENOUS IMMUNOGLOBULIN TREATMENT ON ANTI-GM1 ANTIBODY-MEDIATED NEUROPATHIES

Anti-GM1 antibody may function in disease development in some patients with Guillain-Barre syndrome, chronic inflammatory demyelinating poly radiculoneuropathy and multifocal motor neuropathy. Intravenous immuno globulin (IVIg) therapy is effective in these neuropathies, but the me chanism by which IVIg acts is not clear. To test whether it has anti-i diotypic activity on anti-GM1 antibody, we investigated whether IVIg i nhibits the binding of cholera toxin to GM1. It inhibited the reaction between cholera toxin and GM1 mediated by F(ab')(2) fragments of IgG. Treatment with sialidase did not inhibit the binding of cholera toxin to GM1, whereas denaturation with guanidine did. This suggests that t he GM1 epitope in IVIg has peptide and not carbohydrate structures. Th e variable region of IVIg may bind to anti-GM1 antibody, as well as to cholera toxin, thereby neutralizing the pathogenic effects of the aut oantibody.