Abstract
Immunotherapy using an antibody (rituximab) targeting CD20 antigen in combination with chemotherapy has been recently associated with significantly improved response rate and survival in patients with various types of CD20-positive B-cell lymphoproliferative disorders. This treatment may induce the disappearance of CD20 surface expression on neoplastic B-cells. Several mechanisms have been proposed to explain CD20 loss after rituximab therapy, while the clinical significance (if any) of this phenomenon is still not clear. We have produced a brief overview of the biological aspects of CD20 modulation after rituximab treatment and its possible clinical implications.