Role of parasite surface glycoconjugates on induction/regulation of immune responses and inflammation, elicited during Trypanosoma cruzi infection: potential implications on pathophysiology of Chagas" disease

RESUMO

To understand the interaction of Trypanosoma cruzi and the immune system of the vertebrate host, and therefore the pathophysiology of Chagas' disease, different research groups have focused their attention on the identification and characterization of parasite molecules involved in the activation of either innate or adaptive immune responses. The parasite surface molecules that serve as targets of the vertebrate host immune system have also been studied and identified. These studies have revealed that the quatitatively dominant complex of glycosylphosphatidylinositol (GPI)-anchored molecules (GIPLs, mucins and TS) present on the surface of T. cruzi trypomastigotes are essential to control activation of the innate immune system and promote initiation of acquired immune responses in the vertebrate host. Two major families of surface glycoproteins (mucin-like glycoproteins and transialidases) have also been shown to be important targets of parasite specific humoral and cellular immune responses. They are, thus, important candidates for vaccine development as determined in studies using experimental models. Studies regarding the molecular cloning and/or biochemical characterization of the above mentioned T. cruzi surface molecules, and their ability to influence the outcome of T. cruzi infection in the vertebrate host through the stimulation and/or control of the immune system are presently reviewed. A proposition is made that such molecules may have evolved and been selectively conserved to establish an equilibrium between the parasite and its vertebrate host, limiting parasite replication, but allowing parasite persistence and host survival, thus favoring the maintenance of T. cruzi life cycle.