We propose to study the mechanisms of antibody dependent suppression of acute myelogenous leukemia (AML) in a rat model system. We have a number of monoclonal antibodies (McAb) of the IgM isotype all of which consistently cause leukemia suppression in vivo. Our preliminary studies suggest that complement (C) may play a role in this reaction. We, therefore, plan to: (1) extend our preliminary observations to further evaluate the role of C in leukemia suppression; (2) investigate whether a number of different IgM McAb that cause leukemia suppression also require the participation of C; (3) investigate the possible involvement of effectors in addition to C; and (4) investigate whether agents thst stimulate the reticuloendothelial system (RES) can enhance leukemia suppression. We believe that the availability of McAb and an understanding of the effector mechanisms should enhance the potential of immunotherapy of AML in human patients. (HF)
