Abstract: Epidemiologic coincidence initiated our interest in studying the interactions between environmental mercury exposures and host response to pathogen infection. In both human populations and murine models of malaria, Hg increases parasitemia after infection. In mice, Hg also blocks acquisition of immunity; preliminary evidence in human populations in the Amazon is consistent. Further studies indicate that Hg at subcytotoxic levels of exposure may interfere with hepatic mechanisms of immune response, specifically the coupling between Antigen Presenting Cells and production of interferon-gamma, as well as Th-1 related mechanisms regulating macrophage production of NO. Current research is directed towards understanding Th-1 and Th-2 related events in Hg immunotoxicity, with both immunosuppression and autoimmunity as functional outcomes of exposure.