Acquired immunodeficiency syndrome‐associated lymphomas are efficiently lysed through complement‐dependent cytotoxicity and antibody‐dependent cellular cytotoxicity by rituximab

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Abstract
Summary. Rituximab (Mabthera) and alemtuzumab (Campath®, Mabcampath®) are non‐conjugated IgG1 therapeutic monoclonal antibodies directed against the CD20 and CD52 surface antigens respectively. They are presently used in the therapy of indolent B‐cell non‐Hodgkin's lymphoma (B‐NHL) and of B‐cell chronic lymphocytic leukaemia, and are thought to act mainly through complement‐dependent cytotoxicity (CDC) and antibody‐dependent cellular cytotoxicity (ADCC). Here we have analysed the capacity of these two monoclonal antibodies to lyse cell lines of acquired immunodeficiency syndrome (AIDS)‐related B‐NHL through either complement activation or antibody‐dependent cytotoxicity. Rituximab strongly activated both CDC and ADCC against CD20‐positive AIDS‐NHL cells lines, inducing up to 60–98% and 20% specific lysis respectively. In contrast, alemtuzumab was a poor activator of CDC, even in the AIDS‐NHL cell lines expressing high amounts of CD52, leading to a lysis of only 1–30%, whereas it was at least as strong as rituximab in inducing ADCC of the same lines (up to 30% specific lysis). Altogether, these data offer a first in vitro rationale supporting the therapeutic use of rituximab for CD20‐positive AIDS‐NHL.