Alemtuzumab is a humanized monoclonal antibody that selectively targets CD52 to deplete circulating T and B lymphocytes, thought to be critical mediators of MS inflammatory processes. Alemtuzumab has shown efficacy superior to subcutaneous interferon beta-1a in two phase III clinical trials conducted in relapsing-remitting MS patients. Following alemtuzumab treatment, a distinctive pattern of T and B cell repopulation begins within weeks, potentially leading to a rebalancing of the immune system. To explore the mechanism of action of alemtuzumab, human CD52 transgenic mice were used to evaluate alemtuzumab-mediated depletion and repopulation of lymphocytes in circulation as well as within lymphoid tissues.  In addition, the impact of alemtuzumab on the immune status of treated mice was also examined. To expand our understanding of anti-CD52 therapy in the context of disease, an antibody against murine CD52 was generated and its activity was evaluated in an EAE mouse model of multiple sclerosis.

Preclinical and clinical evaluation of alemtuzumab in multiple sclerosis

245th National Meeting (2013)

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