Open Access#12013
Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation
This paper identifies the mechanism by which patients with multiple sclerosis develop secondary autoimmunity after treatment with the lymphocyte-depleting humanized monoclonal antibody alemtuzumab (Campath-1H). In identifying this mechanism, it shows that T-cell homeostatic proliferation can lead to autoimmunity in humans. Alemtuzumab is one of the most effective treatments of multiple sclerosis tested to date; it is currently licensed in the European Union and under consideration by the Food and Drug Administration. Understanding what drives its most significant side effect is of clear clinical importance.