alexa Insights into the Mechanisms of the Therapeutic Efficacy of Alemtuzumab in Multiple Sclerosis
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
Open Access

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Review Article

Insights into the Mechanisms of the Therapeutic Efficacy of Alemtuzumab in Multiple Sclerosis

Mark S Freedman1, Johanne M Kaplan2 and Silva Markovic-Plese3*
1University of Ottawa, Multiple Sclerosis Research Clinic, the Ottawa Hospital-General Campus, Ottawa, Ontario K1H 8L6, Canada
2Genzyme, a Sanofi Company, Framingham, MA 01701, USA
3Department of Neurology, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, NC 27599-7025, USA
Corresponding Author : Silva Markovic-Plese, MD, PhD
University of North Carolina at Chapel Hill
105 Mason Farm Road, Neuroscience Research Building
Room 6129, Chapel Hill, NC 27599, USA
Tel: 919 966 3701
Fax: 919 843 4576
E-mail: [email protected]
Received May 24, 2013; Accepted July 01, 2013; Published July 08, 2013
Citation: Freedman MS, Kaplan JM, Markovic-Plese S (2013) Insights into the Mechanisms of the Therapeutic Efficacy of Alemtuzumab in Multiple Sclerosis. J Clin Cell Immunol 4:152. doi:10.4172/2155-9899.1000152
Copyright: © 2013 Freedman MS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

The pathogenesis of multiple sclerosis (MS) is thought to involve peripheral activation of immune cells against central nervous system (CNS) antigens and their migration across the blood–brain barrier, leading to CNS inflammation and neurodegeneration. Alemtuzumab, a humanized anti-CD52 monoclonal antibody that rapidly depletes CD52- expressing cells from the circulation, is being investigated as a new treatment option in relapsing-remitting MS (RRMS). Clinical and radiologic results indicate robust suppression of inflammation related to the depletion of T and B lymphocytes during each treatment course of alemtuzumab. Furthermore, several lines of evidence suggest that the long-term clinical effects of alemtuzumab are attributable to qualitative changes in repopulating lymphocyte subsets potentially leading to a rebalancing of the immune system. Here, we review the contribution of data from animal models, ex vivo human studies, and clinical trials to the understanding of the mechanisms underlying the therapeutic effect of alemtuzumab in patients with RRMS.

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