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Article type: Research Article
Authors: Elkarim, Rihab A.a | Mustafa, Mahaa | Link, Hamsa | Bakhiet, Moiza; * | Ekerfelt, Christinab | Vrethem, Magnusb | Ernerudh, Janb
Affiliations: [a] Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden. Tel.: + 46 8 58582276 | [b] Department of Neurology and Transfusion Medicine and Clinical Immunology, University Hospital, Linköping, Sweden. Tel.: + 46 13 222000
Correspondence: [*] Correspondence to: Moiz Bakhiet, MD, Ph.D., Division for Neurology, Huddinge University Hospital (R54) S-141 86 Huddinge, Sweden. Tel.: + 46 8 58582276; Fax: + 46 8 7744822; E-mail: Moiz.Bakhiet@cnsf.ki.se
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.
Keywords: polyneuropathy, monoclonal gammopathy, autoantibody, IFN-γ, cytokine
DOI: 10.3233/HAB-1999-9106
Journal: Human Antibodies, vol. 9, no. 1, pp. 55-60, 1999
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