The CD52 antigen, which is targeted by alemtuzumab, is highly expressed on mature T
lymphocytes, monocytes and monocyte-derived dendritic cells as well as on mature B cells. Due
to its more promiscuous effect on immune cells, alemtuzumab not only targets antibody
producing B lymphocytes as does rituximab, but also targets alloreactive T lymphocytes and
dendritic cells that also contribute to the complex pathogenesis of chronic GVHD.
Our hypothesis is that alemtuzumab will be effective in the treatment of chronic GVHD through
its promiscuous depletion of alloreactive T lymphocytes, dendritic cells as well as antibody
producing mature B-lymphocytes.