Abstract We found a defective suppressor cell function in vitro both in idiopathic chronic inflammatory demyelinating polyneuropathy and in paraproteinemic neuropathy with antibodies to sulfated glucuronyl paragloboside. In the presence of interferon β, suppressor cell function was normalized. Our results suggest that a decreased suppressor cell function plays a pathogenetic role in dysimmune neuropathies. Interferon β might represent an adjunctive therapy in CIDP both acting on a defective blood–nerve barrier and normalizing an otherwise defective suppressor cell function. Keywords Chronic inflammatory demyelinating polyneuropathy; Myelin associated glycoprotein; Sulfated glucuronyl paragloboside; Suppressor cell function; Recombinant human IFNβ1a