ABSTRACT
M acrophages serve either as host and primary effector cells against Trypanosoma cruzi, the protozoan parasite responsible for Chagas disease. Although the parasite mobilizes innate and adaptive immune responses that induce macrophage activa tion and keep infection under control, T. cruzi persists in the host for life. Parasite persistence is associated with inflammatory destruction of skeletal and cardiac muscle. Here, the roles of T cruzi molecules and immune mechanisms involved in parasite evasion of macrophage defenses are discussed. Targeting these molecules and mechanisms will be essential for attaining success ful therapies and vaccination.
