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International Immunology Advance Access originally published online on August 6, 2008
International Immunology 2008 20(10):1313-1319; doi:10.1093/intimm/dxn086
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Glatiramer acetate treatment does not modify the clinical course of (NZB x BXSB)F1 lupus murine model

Paula Borel1, Mahdia Benkhoucha1,2, Martin S. Weber3,4, Scott S. Zamvil3, Marie-Laure Santiago-Raber1 and Patrice H. Lalive1,2

1 Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Michel Servet 1, 1211 Geneva 4, Switzerland
2 Department of Neurosciences, Division of Neurology, Neuroimmunology Laboratory, University Hospital of Geneva, Geneva, Switzerland
3 Department of Neurology, University of California, San Francisco, CA, USA
4 Department of Neurology, Technische Universität München, Munich, Germany

Correspondence to: P. H. Lalive; E-mail: patrice.lalive{at}hcuge.ch

Glatiramer acetate (GA, copolymer-1, Copaxone®), a therapy approved for treatment of multiple sclerosis (MS), prevents and reverses experimental autoimmune encephalomyelitis, the animal model of MS. In central nervous system autoimmune disease, GA is thought to act through modulation of antigen-presenting cells, such as monocytes, mediating an antigen-independent Th2 shift and development of FoxP3+ regulatory T cells. Recent reports indicate that GA may also be effective in models of other autoimmune diseases such as uveoretinitis, inflammatory bowel disease and graft rejection. To date, the potential effect of GA in lupus animal models has not been described. (NZB x BXSB)F1, male mice bearing Y-linked autoimmune acceleration , is a lupus-prone mouse model which is associated with a monocytosis accelerating disease progression. These mice were treated with GA before disease onset until death and both mortality rate and biological parameters were assessed to investigate whether GA may be beneficial in this spontaneous model of systemic lupus erythematosus. GA exerted no beneficial effect on the median survival after up to 7 months of treatment. Humoral and cellular parameters used as markers for lupus progression, such as anti-chromatin, anti-double-stranded DNA and anti-erythrocytes antibodies, hematocrit and monocytosis, were similarly unchanged. Our study demonstrates that GA has no significant effect on the progression of the (NZB x BXSB)F1 lupus-prone animal model. These results reinforce the hypothesis that GA may exert its beneficial effect in some specific autoimmune diseases only.

Keywords: Copaxone®, experimental autoimmune encephalitis, (NZB x BXSB)F1 lupus-prone animal model, systemic lupus erythematosus, Y-chromosome-associated accelerator

Transmitting editor: I. Pecht

Received 7 February 2008, accepted 9 July 2008.


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D. Burger, N. Molnarfi, M. S. Weber, K. J. Brandt, M. Benkhoucha, L. Gruaz, M. Chofflon, S. S. Zamvil, and P. H. Lalive
Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1{beta} in human monocytes and multiple sclerosis
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