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Interferon-: A Therapeutic for Autoimmune Lupus in MRL-Fas^lpr Mice

Andreas Schwarting^*, Kathrin Paul^*, Stefan Tschirner^*, Julia Menke^*, Torsten Hansen, Walburgis Brenner, Vicki Rubin Kelley, Manfred Relle^* and Peter R. Galle^*

^* First Department of Medicine, Institute of Pathology, and Department of Urology, Johannes Gutenberg-University Mainz, Mainz, Germany; and Renal Division, Brigham & Women’s Hospital, Boston, Massachusetts

Address correspondence to: Dr. Andreas Schwarting, First Department of Medicine, Johannes-Gutenberg University of Mainz, Langenbeckstrasse 1, Mainz 55131, Germany. Phone: +49-6131-17-2666; Fax: +49-6131-17-6621; aschwart{at}mail.uni-mainz.de

Received for publication November 30, 2004. Accepted for publication August 18, 2005.

Type I interferons are associated with lupus. Genes that are regulated by IFN- are upregulated in pediatric lupus patients. Gene deletion of the IFN-/ receptor in experimental lupus-like NZB mice results in reduced disease activity. Conversely, IFN- is a well-established treatment in multiple sclerosis, another autoimmune disease. For determining whether IFN- treatment is harmful or beneficial in lupus, MRL-Fas^lpr mice were injected with this type I IFN. Treatment was initiated in MRL-Fas^lpr mice with mild and advanced disease. IFN- was highly effective in prolonging survival and ameliorating the clinical (renal function, proteinuria, splenomegaly, and skin lesions), serologic (autoantibodies and cytokines), and histologic parameters of the lupus-like disease in mice that had mild and advanced disease. Several underlying mechanisms of IFN- therapy involving cellular (decreased T cell proliferation and infiltration of leukocytes into the kidney) and humoral (decrease in IgG3 isotypes) immune responses and a reduction in nephrogenic cytokines were identified. In conclusion, IFN- treatment of lupus nephritis in MRL-Fas^lpr mice is remarkably beneficial and suggests that IFN- may be an appealing therapeutic candidate for subtypes of human lupus.

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