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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4607v1 106/5/1875    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Herrmann, M. M. Articles by Weissert, R. Search for Related Content PubMed PubMed Citation Articles by Herrmann, M. M. Articles by Weissert, R. Related Collections Immunobiology Transplantation Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSPLANTATION Tolerance induction by bone marrow transplantation in a multiple sclerosis model Martin M. Herrmann, Susanne Gaertner, Christine Stadelmann, Jens van den Brandt, Robert Böscke, Wilfried Budach, Holger M. Reichardt, and Robert Weissert From the Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Germany; Department of Neuropathology, University of Göttingen, Germany; Molecular Immunology, Institute of Virology and Immunobiology, University of Würzburg, Germany; and Department of Radiooncology, University of Tübingen, Germany. Experimental autoimmune encephalomyelitis (EAE) in rats is a highly valuable model of multiple sclerosis (MS) because 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, and 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, rats receiving bone marrow (BM) transplants were protected from subsequently induced relapses. These findings could be confirmed by histopathology in which rats receiving BM transplants did not have lesions compared with controls not receiving transplants. Importantly, the protective effect was achieved by allogeneic, syngeneic, and BM 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 rechallenge 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. (Blood. 2005;106:1875-1883) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. A. Meadows and D. L. Bhatt Clinical Aspects of Platelet Inhibitors and Thrombus Formation Circ. Res., May 11, 2007; 100(9): 1261 - 1275. [Abstract] [Full Text] [PDF] D. Tischner, A. Weishaupt, J. v. d. Brandt, N. Muller, N. Beyersdorf, C. W. Ip, K. V. Toyka, T. Hunig, R. Gold, T. Kerkau, et al. Polyclonal expansion of regulatory T cells interferes with effector cell migration in a model of multiple sclerosis Brain, October 1, 2006; 129(10): 2635 - 2647. [Abstract] [Full Text] [PDF] M. A. Friese, X. Montalban, N. Willcox, J. I. Bell, R. Martin, and L. Fugger The value of animal models for drug development in multiple sclerosis Brain, August 1, 2006; 129(8): 1940 - 1952. [Abstract] [Full Text] [PDF]

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