Immune mechanisms of new therapeutic strategies in multiple sclerosis-A focus on alemtuzumab

Clin Immunol. 2012 Jan;142(1):25-30. doi: 10.1016/j.clim.2011.04.006. Epub 2011 Apr 15.


Alemtuzumab is a humanized monoclonal antibody targeting CD52, a broadly expressed cell surface molecule on immune cells. Application results in a rapid and long-lasting removal of lymphocyte populations from the circulation. Alemtuzumab-treatment of MS patients with relapsing-remitting forms of the disease significantly reduced the risk of relapse and accumulation of disability compared to interferon β-1a treatment in a phase II trial. Interestingly, further analysis together with parallel experimental studies suggested that alemtuzumab not only reduces disease activity due to its immune cell-depleting effect, but also confers neuroprotective effects, presumably by inducing production of neurotrophic factors in autoreactive T cells. However, alemtuzumab-treated MS patients experienced increased rates of novel autoimmunity and a slight increase in infections, demonstrating that alemtuzumab-mediated skewing of the immune cell compartment has a broad influence on immune functions. This review discusses the current concepts about the underlying mechanisms causing these altered immune responses in alemtuzumab-treated MS patients.

Publication types

  • Review

MeSH terms

  • Alemtuzumab
  • Animals
  • Antibodies, Monoclonal, Humanized / immunology
  • Antibodies, Monoclonal, Humanized / pharmacology*
  • Antibodies, Neoplasm / immunology
  • Antibodies, Neoplasm / pharmacology*
  • Clinical Trials as Topic
  • Humans
  • Immunosuppressive Agents / immunology
  • Immunosuppressive Agents / pharmacology*
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Multiple Sclerosis, Relapsing-Remitting / immunology


  • Antibodies, Monoclonal, Humanized
  • Antibodies, Neoplasm
  • Immunosuppressive Agents
  • Alemtuzumab