This review highlights that Chagas cardiomyopathy is driven by distinct immune mechanisms: acute destruction via targeted parasite antigens and chronic progressive damage via CD4+ T cell-mediated autoimmunity.
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May inform phase-specific immunomodulation in Chagas cardiomyopathy; leaves open clinical translation pending interventional studies.
The mechanisms by which Trypanosoma cruzi causes cardiomyopathy and induces neuronal destruction are discussed in this paper. The results suggest that autoimmunity in the chronic phase is the main cause of the progressive cardiac destruction, and that autoreactivity is restricted to the CD4+ T cell compartment. During the acute phase, the neuronal and cardiac fiber destruction occurs when ruptured parasite nests release T. cruzi antigens that bind to the cell surface in the vicinity which become targets for the cellular and humoral immune response against T. cruzi. The various factors involved in the genesis of autoimmunity in chronic T. cruzi infection include molecular mimicry, presentation of self-antigens and imbalance of immune regulation.
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Soares et al. (1999) studied this question.
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