Antibody-dependent cell-mediated cytotoxicity in reinfection immunity to schistosomes in the rat involves either IgG2a anaphylactic antibody and eosinophils or IgE antibody and macrophages. The first system requires two signals, one by the antibody through the eosinophil Fc receptor, another by mast cells through the release of mediators among which is ECF-A. IgE antibody complexed with schistosome antigen binds to an IgE-specific receptor on the macrophage and triggers the cell to release enzymes and superoxide. Immunity in rat schistosomiasis is antibody-dependent, abolished in anti-µ treated neonate rats or by passive serum transfer after selective depletion of either IgG2a or IgE. The two anaphylactic antibody-dependent cell cytotoxicity systems are in a permanent balance in immune rats, eosinophils being blocked by IgG2a immune complexes when this cell is inefficient. Anaphylactic antibodies thus play a key role in triggering and modulating effector cell function.