The importance of aberrant T-cell responses in Chagas disease

George A DosReis1, Celio G Freire-de-Lima, Marise P Nunes

  • 1Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Centro de Ciências da Saúde, Bloco G, Rio de Janeiro 21949-900, Brazil. gdosreis@biof.ufrj.br

Trends in Parasitology
|April 20, 2005
PubMed

Insights

Mechanisms of aberrant T-cell activation drive Trypanosoma cruzi persistence and cardiac injury in Chagas disease. Host cell apoptosis promotes parasite replication and inflammation, leading to heart damage.

Area of Science:

  • Immunology
  • Parasitology
  • Cardiology

Background:

  • Chagas disease, caused by Trypanosoma cruzi, leads to heart damage.
  • Aberrant T-cell activation is implicated in Trypanosoma cruzi persistence and cardiac injury.

Purpose of the Study:

  • To discuss recently identified mechanisms of aberrant T-cell activation.
  • To explore the role of host cell apoptosis in Trypanosoma cruzi replication and cardiac inflammation.

Main Methods:

  • Review of recent findings on T-cell activation mechanisms.
  • Analysis of the role of apoptosis in parasite replication.
  • Examination of immune responses initiated by phagocytic removal of infected cells.

Main Results:

  • Host cell apoptosis drives Trypanosoma cruzi replication in macrophages.
  • Apoptosis is a feature of cardiac inflammation in Chagas disease.
  • Phagocytic removal of infected apoptotic cardiomyocytes and innate immune receptor signaling initiate damaging immune responses.

Conclusions:

  • Aberrant T-cell activation contributes to Trypanosoma cruzi persistence.
  • Host cell apoptosis plays a critical role in cardiac injury during Chagas disease.
  • Immune responses initiated by phagocytosis of infected apoptotic cells are key to heart damage.

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