Alemtuzumab, formally known as Campath-1H, is a humanized monoclonal antibody 
directed against CD52, a protein on the surface of lymphocytes and monocytes 
with unknown function. A single dose of alemtuzumab leads to a rapid, profound 
and prolonged lymphopenia. A Phase II trial has shown that alemtuzumab reduces 
the risk of relapse and accumulation of disability by over 70% compared with 
interferon beta in patients with early relapsing-remitting multiple sclerosis 
(MS). Alemtuzumab has been used in Cambridge as an experimental treatment for MS 
since 1991. In this review we summarize our experience; describing how this 
prototypical, "bench-to-bedside" therapy continues to inform basic science, 
revealing aspects of the pathogenesis of MS and lymphopeniaassociated 
autoimmunity.