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.