Although the cytostatic or cytotoxic activity of macrophages against tumour cells has been known for almost 20 years it is only recently that precise attention has been paid to the effector function of macrophages in immunity to helminths. The increase in interest in this cytotoxic potential came from the evidence provided by in vitro studies in many laboratories since 1974, which showed (a) that cytotoxic T cells played a negligible if any, role in killing parasites (BUTTERWORTH et al., 1979), and (b) that the pre-eminent role was played by bhagocytic cell populations, including macrophages, eosinophils and neutronhils KAPRON et al.. 1982). One of the maior pieces-of information gained from such studies has been the demonstration of the precise interaction between specific antibodies and the effector cell concerned. It is, however, also noteworthy that our increased knowledge of the processes of cell activation (COHN, 1978) has not been accompanied by similar progress in our knowledge of the molecular mechanisms leading to the death of a multicellular organism. It should also be stressed that, so far, all the information available has come from in vitro studies, the in vivo effector function of macrophages, as for other phagocytic cells, remaining unclear. From a general standpoint, there are, in theory, many ways in which a macrophage could have a cytotoxic effect on a natural metazoan parasite. There are, for example, reports that some natural killer activity can be detected (ELLNER & MAHMOUD, 1979) or that opsonized targets in the presence of complement can be efficienily damaged(PEREZ & SMMITHERS. 1977). However. there has been little documentation of these mechanisms whereas two processes of activation, one non-specific mediated by lvmohokines. the other snecific mediated bv IeE antibody, have retained much attention. While the classical pathway of macrophage activation by lymphocyte factors has already been known in nonparasitic systems (COHN, 1978; BOUT & DAVID, 1980), hehninth models have provided evidence that binding antibodies or immune complexes to appropriate macrophage receptors could turn the cell into a specific effector cell.