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https://www.arca.fiocruz.br/handle/icict/5635
IMMUNOPATHOLOGY OF CARDIOMYOPATHY IN THE EXPERIMENTAL CHAGAS DISEASE
Cardiomiopatia Chagásica/imunologia
Trypanosoma cruzi/imunologia
Animais
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Linhagem Celular
Cardiomiopatia Chagásica/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Miocárdio/imunologia
Miocárdio/patologia
Neurônios/imunologia
Neurônios/patologia
Affilliation
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil.
Abstract
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.
DeCS
Auto-Imunidade/imunologiaCardiomiopatia Chagásica/imunologia
Trypanosoma cruzi/imunologia
Animais
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Linhagem Celular
Cardiomiopatia Chagásica/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Miocárdio/imunologia
Miocárdio/patologia
Neurônios/imunologia
Neurônios/patologia
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