Besides its crucial role in type I hypersensitivity reactions, IgE is involved in anti-parasite immunity. This role has been clearly demonstrated in both human and rat schistosomiasis, but remains controversial in the mouse. Since the cellular distribution of the high affinity IgE receptor, FcεRI, differs in humans and mice, it might explain the differences in effector function of IgE between the two species. In humans, eosinophils and macrophages induce IgE-dependent cytotoxicity toward Schistosoma mansoni larvae, which involves FcεRI in the case of eosinophils. In the present study, we have investigated the expression and function of FcεRI in rat eosinophils and macrophages. We demonstrate, by flow cytometry, fluorescence microscopy, and Western blot analysis, that in rats, as in humans, a functional αγ 2 trimeric FcεRI is expressed on eosinophils and macrophages. We also show that these two cell types can induce IgE-mediated, FcεRI-dependent cellular cytotoxicity toward schistosomula. These results thus provide a molecular basis for the differences observed between rat and mouse regarding IgE-mediated anti-parasite immunity.