Immunity and immune modulation in Trypanosoma cruzi infection
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Published on: January 27, 2019
Fabíola Cardillo1, Rosa Teixeira de Pinho2, Paulo Renato Zuquim Antas2
1Oswaldo Cruz Foundation, Bahia, Rua Waldemar Falcão 121, Salvador 40295-001, Brazil.
Insights
Chagas disease, caused by Trypanosoma cruzi, involves complex immune responses. Understanding these interactions is key to developing new therapies and vaccines for this parasitic infection.
Area of Science:
- Immunology
- Infectious Diseases
- Parasitology
Background:
- Chagas disease is caused by the protozoan Trypanosoma cruzi.
- The chronic phase can lead to mega syndromes affecting organs like the heart, esophagus, and colon in ~30% of infected individuals.
- Clinical outcomes depend on host-parasite interactions, involving immune responses to parasite and self-antigens.
Purpose of the Study:
- To review findings supporting an integrated immune response in Chagas disease.
- To discuss mechanisms regulating immune responses during chronic infection.
- To highlight the importance of this knowledge for developing novel therapies and vaccines.
Main Methods:
- Review of existing literature on Chagas disease immunology.
- Analysis of host-parasite interactions in lymphoid organs and affected tissues.
- Examination of innate and adaptive immune system roles.
Main Results:
- The immune system, encompassing both innate and adaptive arms, plays a crucial role in controlling Trypanosoma cruzi parasite numbers.
- Mechanisms exist to regulate immune responses, promoting tolerance to residual parasite load during chronic infection.
- Immune responses can be balanced, leading to no disease, or unbalanced, causing inflammation and autoimmune reactions.
Conclusions:
- An integrated view of the immune response is fundamental to understanding Chagas disease progression.
- Knowledge of immune regulation is essential for developing effective therapeutic and vaccine strategies against Trypanosoma cruzi infection.
Abstract:
Chagas disease is caused by the protozoan Trypanosoma cruzi. The parasite reaches the secondary lymphoid organs, the heart, skeletal muscles, neurons in the intestine and esophagus among other tissues. The disease is characterized by mega syndromes, which may affect the esophagus, the colon and the heart, in about 30% of infected people. The clinical manifestations associated with T. cruzi infection during the chronic phase of the disease are dependent on complex interactions between the parasite and the host tissues, particularly the lymphoid system that may either result in a balanced relationship with no disease or in an unbalanced relationship that follows an inflammatory response to parasite antigens and associated tissues in some of the host organs and/or by an autoimmune response to host antigens. This review discusses the findings that support the notion of an integrated immune response, considering the innate and adaptive arms of the immune system in the control of parasite numbers and also the mechanisms proposed to regulate the immune response in order to tolerate the remaining parasite load, during the chronic phase of infection. This knowledge is fundamental to the understanding of the disease progression and is essential for the development of novel therapies and vaccine strategies.
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