Abstract
The cytokine transforming growth factor-β (TGF-β) plays various functions in the control of <b>Trypanosoma cruzi</b> infectivity and in the progression of Chagas' disease. When we immunostained <b>T. cruzi</b>-infected cardiomyocytes (after either <b>in vivo</b> or <b>in vitro</b> infections) for TGF-β, we observed stronger immunoreactivity in parasites than in host cells. TGF-β immunoreactivity evolved during parasite cycle progression, with intense staining in amastigotes versus very faint staining in trypomastigotes. TGF-β was present on the surface of amastigotes, in the flagellar pocket, and in intraparasitic vesicles as revealed by electron microscopy. However, no ortholog TGF-β gene could be identified in the genome of <b>T. cruzi</b> by <b>in silico</b> analysis or by extensive polymerase chain reaction and reverse transcriptase-polymerase chain reaction studies. Immunoreactive TGF-β was most probably taken up by the parasite from the host cell cytoplasm because such an internalization process of biotinylated TGF-β could be observed in axenic amastigotes <b>in vitro</b>. These observations represent the first example of a novel mechanism by which a primitive unicellular protozoan can use host cell TGF-β to control its own intracellular life cycle.
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