Autoimmunity in Chronic Chagas Disease: A Road of Multiple Pathways to Cardiomyopathy?

Elidiana De Bona1, Kárita Cláudia Freitas Lidani1, Lorena Bavia1

  • 1Laboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.

Frontiers in Immunology
|August 22, 2018
PubMed

Insights

Chagas disease, caused by Trypanosoma cruzi, leads to chronic Chagas cardiomyopathy. This review explores how parasite evasion and molecular mimicry may trigger autoimmune responses contributing to disease progression.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Cardiology

Background:

  • Chagas disease (CD) is a neglected tropical disease caused by Trypanosoma cruzi, affecting millions globally and posing a significant public health challenge.
  • Chronic infection establishes, leading to chronic Chagas cardiomyopathy (CCC) due to parasite evasion of the host immune system.
  • T. cruzi persistence generates immune stimuli, causing tissue damage and inflammation, potentially involving autoimmune mechanisms.

Purpose of the Study:

  • To review recent findings and hypotheses on autoimmune mechanisms in the development and progression of chronic Chagas cardiomyopathy (CCC).

Main Methods:

  • This review synthesizes current literature and research hypotheses regarding the autoimmune aspects of Chagas disease progression.
  • Analysis of studies investigating Trypanosoma cruzi evasion strategies and their interaction with the host immune system.
  • Examination of evidence for molecular mimicry and its role in generating autoimmune responses in CD.

Main Results:

  • Trypanosoma cruzi employs immune evasion strategies, allowing persistent infection and chronic inflammation.
  • Molecular mimicry between parasite and host proteins may induce cross-reactivity, leading to autoimmune features like autoantibodies.
  • Evidence suggests a role for autoimmunity in the clinical progression of chronic Chagas cardiomyopathy, although mechanisms remain under investigation.

Conclusions:

  • Autoimmune responses, potentially triggered by parasite persistence and molecular mimicry, are implicated in the pathogenesis of chronic Chagas cardiomyopathy.
  • Further research is needed to elucidate the precise mechanisms driving autoimmunity in human Chagas disease progression.
  • Understanding these autoimmune pathways is crucial for developing targeted therapies for chronic Chagas cardiomyopathy.

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