Intravenous immunoglobulin treatment on anti-GM1 antibodies associated neuropathies inhibits cholera toxin and galectin-1 binding to ganglioside GM1.

Intravenous immunoglobulin (IVIg) therapy is efficacious in some peripheral nervous autoimmune diseases associated with anti-GM1 antibodies. Numerous mechanisms of action have been proposed to account for the immunomodulatory effects of IVIg in immune-mediated diseases. Up to now, the mechanisms of action of IVIg in pathology associated with anti-GM1 antibodies have not been well documented. In the present study, we discovered that IVIg did not inhibit the binding of anti-GM1 antibodies to its antigen and IVIg perfusions did not reduce anti-GM1 antibodies titers. In this observation, we have the result different from the hypothesis of presence of anti-idiotypic antibodies in different IVIg preparations, and show that IVIg inhibits the binding of cholera toxin and galectin-1 to GM1-expressing cells using flow cytometry. Our results suggest that the correct ratio galactosyl/agalactosyl IgG in IVIg interact with macrophages receptors to down-regulate inflammatory function of macrophages and autoimmune diseases in peripheral nerve system.