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Trypanosoma cruzi produces widespread infections in man and animals, parasitizing a variety of cell types, particularly those of the myocardium. In this and other sites, accumulation of lymphocytes and macrophages are common, leading a number of investigators to suggest a role for the macrophage in defense against T. cruzi. This view was disregarded later, when macrophages were seen harboring great numbers of parasites. In the 1950s, Pizzi et al. again stressed the importance of macrophages in T. cruzi infections. They reported on in vivo observations that macrophages from normal mice supported growth of trypomastigotes, whereas in an immunized host, macrophages in inflammatory sites seemed to be capable of destroying those forms. More recently, Hoff described an increased resistance of macrophages from mice infected with T. cruzi and BCG for culture forms of T. cruzi. We have been examining the in vitro interaction of T. cruzi with normal mouse peritoneal macrophages and with macrophages obtained from BCG- and T. cruzi-infected mice.