The immunological mechanisms that control the clinical evolution of Chagas disease are not clear, despite of a better understanding of the mechanisms responsible for the genesis of the cardiac and digestive lesion. Several hypotheses have been proposed in an attempt to explain these phenomena. In this review we discuss the participation of cytokines, chemokines, matrix metalloproteinases, nitric oxide, costimulatory molecules, regulatory T cell, and the new adaptative T helper response–Th17 in determining the clinical forms of
