Abstract
We previously demonstrated the induction of IFN-γ in polyneuropathy patients associated with monoclonal gammopathy, but not in patients with presumably non-immuno-logical types of neuropathy. We herein examined mechanism involving release of neutralizing autoantibodies (Aabs) to IFN-γ in sera from those pateints. In contrast to polyneuropathy patients with monoclonal gammopathy, patients with polyneuropathy of presumably non-immunological types showed increased production of neutralizing Aabs specific for IFN-γ. These results demonstrate a role for autoimmunity in cytokine regulation. However, their association to the clinical manifestations of the disease requires further investigations, which are necessary for future consideration in therapeutic strategies.
Get full access to this article
View all access options for this article.
