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Immunomodulation of murine experimental SLE-like disease by interferon-

Y Levi

M Blank

Research Unit of Autoimmune Diseases and the Department of Medicine ‘B’, Sheba Medical Center, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

V Barak

Laboratory of Tumor Immunology, The Hebrew University & Hadassah Medical School, Jerusalem, Israel

P Langevitz

Unit of Rheumatology and the Department of Medicine ‘F’

A Afek

The Institute of Pathology, Sheba Medical Center, Tel-Hashomer, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

F Nicoletti

Department of Medical Pathology and Metabolic Diseases, Catania, Italy

J Kopolovic

The Institute of Pathology, Sheba Medical Center, Tel-Hashomer, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

B Gilburd

Research Unit of Autoimmune Diseases and the Department of Medicine ‘B’, Sheba Medical Center, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

P L Meroni

Institute of Internal Medicine, Infectious Diseases and Immunopathology, IRCCS Policlinico-University of Milan, Italy

Y Shoenfeld

Research Unit of Autoimmune Diseases and the Department of Medicine ‘B’, Sheba Medical Center, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

The objective of this study was to assess the impact of murine recombinant IFN- and anti-IFN- monoclonal antibody on the BALB/c mice experimental model of lupus. BALB/c female mice were immunized with a human anti-DNA antibody that carries the 16=6 idiotype. These mice were divided into several therapeutic groups according to different treatment strategies; injection with mouse recombinant IFN-, anti-IFN- mAb, phosphate-buffered saline (PBS), irrelevant mouse IgG and control groups that were neither treated nor immunized with the human anti-DNA antibody.

The administration of IFN- intensified the degree of clinical, histological and serological parameters in this model of BALB/c murine lupus. This immunomanipulation decreased the mice longevity. All the laboratory parameters reflected acceleration of the disease in the IFN- treated group as an elevated sedimentation rate, decreased white blood cell count and the development of massive proteinuria. One month after the boost injection, all the mice that were immunized with the anti-DNA antibody, developed high titers of autoantibodies; however, following an additional month, their levels declined in the IFN- treated group. These findings were in concordance with an increased glomerular deposition of immune complexes in the IFN- treated mice. IFN- upregulated the levels of IL-4 and increased the number of IL-4 and IL-6 secreting splenocytes.

In conclusion IFN- administration can aggravate the clinical and laboratory outcome of 16=6id induced lupus in BALB/c mice.

Key Words: systemic lupus erythematosus • IFN- • Th1 cells • Th2 cells • cytokines

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