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-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy. Intravenous immunoglobulin (IVIg) therapy is effective in these neuropathies, but the mechanism by which IVIg acts is not clear. To test whether it has anti-idiotypic activity on anti-GM1 antibody, we investigated whether IVIg inhibits 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 the GM1 epitope in IVIg has peptide and not carbohydrate structures. The variable region of IVIg may bind to anti-GM1 antibody, as well as to cholera toxin, thereby neutralizing the pathogenic effects of the autoantibody.
Yuki
N
N
Department of Biochemistry, Faulty of Medicine, Tokyo Medical and Dental University, Japan.
Miyagi
F
F
D000937:Antigen-Antibody Reactions; D001323:Autoantibodies / Q000276:immunology*; D002772:Cholera Toxin / Q000276:immunology; D005677:G(M1) Ganglioside / Q000276:immunology*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000494:pharmacology* / Q000627:therapeutic use*; D007700:Kinetics; D009443:Neuritis / Q000276:immunology* / Q000628:therapy*; D011129:Polyradiculoneuropathy / Q000276:immunology / Q000628:therapy
D001323:Autoantibodies; D016756:Immunoglobulins, Intravenous; D005677:G(M1) Ganglioside; D002772:Cholera Toxin