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.