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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
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.
Abstract:
Persistence of Trypanosoma cruzi is associated with damage to the heart, which is a characteristic of Chagas disease. In this article, we discuss recently identified mechanisms of aberrant T-cell activation that are responsible for persistence of T. cruzi and cardiac injury. Among them, apoptosis of host cells drives T. cruzi replication in macrophages and is present in cardiac inflammation. It is proposed that phagocytic removal of infected apoptotic cardiomyocytes, combined with signaling through innate immune receptors, is required to initiate immune responses that damage the heart.
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