ABSTRACT
The clinical phenomenon of the graft-versus-leukemia (GVL) effect is linked to predictions made a century ago that immune reactivity could be used beneficially as an antitumor mechanism. Distinct perspectives led Ehrlich to propose a ‘‘magic bullet,’’ Metchnikoff to pursue the potent phagocyte, and Coley to pursue bacterial toxins as antitumor activators [1]. With over one hundred years of data and progress, these three philosophies are now best visualized in the mechanisms of (1) T cell-and antibody-mediated tumor recognition, as magic bullets of sorts; (2) macrophages, natural killer cells, granulocytes, and the diverse functions associated with the ‘‘innate’’ immune system [2]; and (3) therapeutic utilization of recombinant cytokines or cytokine activators.
