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J. W. Peterson, L. Bo, S. Mork, A. Chang, R. M. Ransohoff and B. D. Trapp,“VCAM-1 Positive Microglia Target Oligodendrocytes at the Border of Multiple Sclerosis Lesions,” Journal of Neuropathology & Experimental Neurology, Vol. 61, No. 6, 2002, pp. 539-546.

has been cited by the following article:

• TITLE: Alemtuzumab: A Place in Therapy for Treatment of Multiple Sclerosis

  AUTHORS: Teya M. Tietje, Douglas R. Allington, Michael P. Rivey

  KEYWORDS: Alemtuzumab; Multiple Sclerosis; Monoclonal Antibody; Lymphocyte Depletion

  JOURNAL NAME: International Journal of Clinical Medicine, Vol.4 No.10, October 25, 2013

  ABSTRACT: Alemtuzumab is a humanized mononclonal antibody known to cause rapid depletion of B-and T-cell lymphocytes. Subsequent repletion of these lymphocytes leads to changes in adaptive immunity. Alemtuzumab is approved by the United States Food and Drug Administration (FDA) for the treatment of B-cell lymphocytic leukemia but has been investigated off-label in recent years for treatment of autoimmune diseases, including multiple sclerosis (MS). In MS treatment, alemtuzumab is administered as pulsed therapy, given once daily initially for 5 consecutive days and then for 3 consecutive days at 12-month intervals. Alemtuzumab has recently been compared to interferon beta 1-a in one phase II and two phase III trials in patients with relapsing-remitting MS. Results from the studies show alemtuzumab compared to interferon beta 1-a is associated with a greater reduction in the risk of sustained accumulation of disability and is more effective in reducing disease relapse rates. The treatment of MS continues to be a healthcare challenge due to the modest clinical benefit and adverse effect profiles of available disease modifying treatment options. Available data suggest alemtuzumab may offer better efficacy outcomes compared to traditional disease modifying therapies in patients with MS. However, the agent has not been compared to other new disease modifying medications that have been recently introduced.