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Footpad infection of C3HeB/FeJ mice with  Leishmania amazonensis  leads to chronic lesions accompanied by large parasite loads. Co-infecting these animals with  L. major  leads to induction of an effective Th1 immune response that can resolve these lesions. This cross-protection can be recapitulated in vitro by using immune cells from  L. major -infected animals to effectively activate  L. amazonensis -infected macrophages to kill the parasite. We have shown previously that the B cell population and their IgG2a antibodies are required for effective cross-protection. Here we demonstrate that, in contrast to  L. major , killing  L. amazonensis  parasites is dependent upon FcRγ common-chain and NADPH oxidase-generated superoxide from infected macrophages. Superoxide production coincided with killing of  L. amazonensis  at five days post-activation, suggesting that opsonization of the parasites was not a likely mechanism of the antibody response. Therefore we tested the hypothesis that non-specific immune complexes could provide a mechanism of FcRγ common-chain/NADPH oxidase dependent parasite killing. Macrophage activation in response to soluble IgG2a immune complexes, IFN-γ and parasite antigen was effective in significantly reducing the percentage of macrophages infected with  L. amazonensis . These results define a host protection mechanism effective during  Leishmania  infection and demonstrate for the first time a novel means by which IgG antibodies can enhance killing of an intracellular pathogen.

An In Vitro Model of Antibody-Enhanced Killing of the Intracellular Parasite Leishmania amazonensis