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Blood, 1 September 2005, Vol. 106, No. 5, pp. 1875-1883.
Prepublished online as a Blood First Edition Paper on May 17, 2005; DOI 10.1182/blood-2004-12-4607.
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Submitted December 8, 2004
Accepted May 10, 2005
Tolerance induction by bone marrow transplantation in a multiple sclerosis model
Martin M Herrmann, Susanne Gaertner, Christine Stadelmann, Jens van den Brandt, Robert Boscke, Wilfried Budach, Holger M Reichardt, and Robert Weissert*
Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Department of Neuropathology, University of Gottingen, Gottingen, Germany
Molecular Immunology, Institute of Virology and Immunobiology, University of Wurzburg, Wurzburg, Germany
Department of Radiooncology, University of Tubingen, Tubingen, Germany
* Corresponding author; email: robert.weissert{at}uni-tuebingen.de.
Experimental autoimmune encephalomyelitis (EAE) in rats is a highly valuable model of multiple sclerosis (MS) since it mimics major hallmarks of the human disease. EAE induced with myelin-oligodendrocyte-glycoprotein (MOG) in DA rats is relapsing-remitting and lesions in the central nervous system show inflammation, demyelination, axonal and neuronal loss. Recently, bone marrow transplantation (BMT) was introduced as a novel strategy to treat MS but its efficiency and the underlying mechanism are debatable. In MOG induced EAE we found that BMT at the peak of EAE but not in the chronic phase leads to disease attenuation. In both settings bone marrow (BM) transplanted rats were protected from subsequently induced relapses. These findings could be confirmed by histopathology in which BM transplanted rats did not have lesions compared to non-transplanted controls. Importantly, the protective effect was achieved by allogeneic, syngeneic and grafts from diseased rats. BMT resulted in increased numbers of CD4+CD25bright regulatory T cells, increased Foxp3 expression, a shift in T cell epitope recognition and a strong reduction of autoantibodies even after re-challenge with MOG. Thus, our results indicate potential mechanisms of how BMT may contribute to the improvement of MS and provide a rationale for its application in patients suffering from various autoimmune diseases.
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