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Protective host response to Trypanosoma cruzi and its limitations

C. Truyens1 and Y. Carlier1,2

1 University Libre de Bruxelles (ULB), Brussels, Belgium, 2Tulane University, New Orleans, LA, United States

Chapter Outline

Innate immune response in T. cruzi infection 580

Soluble components of the innate system 580 Innate recognition of T. cruzi infection 580 Cells of the innate immune system 581

Dendritic cells (DCs) and the initiation of the adaptive immune response 583 Adaptive immune response: induction, characterization, and role of the T cell response 584

T cell epitopes 584

T lymphocytes in the control of the infection 584 Regulatory T cells 585

The recently disclosed role of IL-17 in T cruzi infection 585 Adaptive immune response: the B cell response and production of antibodies 586

Targets of T cruzi-specific Ab 586 Isotypes of specific Ab 586 Effector mechanisms of Ab 587

Deregulations of T and B lymphocyte responses 587

Defective lymphocyte responses 587 Polyclonal activation 588

Escape mechanisms of T. cruzito the immune responses 588

Resistance to complement lysis 588 Intracellular survival 588 Escape from the action of Ab 589

Being a stealth parasite, dampening and disturbing T cell responses 590 Conclusion 590 References 591

T. cruzi induces a complex immune response owing to the simultaneous presence in the vertebrate host of extracellular trypomastigotes disseminating in biological fluids and intracellular amastigotes multiplying in the cytoplasm of a wide variety of cell types, requiring different effector mechanisms to be controlled.

American Trypanosomiasis Chagas Disease. DOI: http://dx.doi.org/10.1016/B978-0-12-801029-7.00026-5

Copyright © 2017 Elsevier Inc. All rights reserved.

Knowledge mainly comes from the experimental mouse model of infection, widely used as the infection progresses similarly in mouse and humans, resulting after the acute parasitemic phase, in chronic parasite persistence. However, experimental data cannot be systematically extrapolated to human infection since mouse and human immune systems display subtle differences.1 In addition, most mouse models uses specific pathogen-free animals, therefore, they are not comparable to humans as they have not experienced other infections responsible for trained immunity.2

This chapter deals with current knowledge on innate and adaptive immune responses involved in the control of acute T. cruzi infection, from initiation to effector mechanisms, as well as immunoregulation and escape mechanisms allowing the parasite to persist lifelong at low levels in tissues. It is an update of the previous edition, in which much more detail and precision can been found.3

 
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