Understanding CD8+ T Cell Immunity to Trypanosoma cruzi and How to Improve It

Rodríguez, Eva V. Acosta; Furlan, Cintia L. Araujo; Vernengo, Facundo Fiocca; Montes, Carolina L.; Gruppi, Adriana

doi:10.1016/j.pt.2019.08.006

Cited by 36 publications

(33 citation statements)

References 110 publications

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“…Although they are ultimately thought to be non‐sterilizing in virtually all cases, 95 it is worth reviewing the key features at the systemic level before we consider the tissue‐specific host‐parasite dynamics at play in the chronic phase. We also refer readers to more in‐depth reviews of adaptive immunity in Chagas disease 46,96,97 …”

Section: Stage 2: Adaptive Responses Take Controlmentioning

confidence: 99%

Host‐parasite dynamics in Chagas disease from systemic to hyper‐local scales

Pérez‐Mazliah

Ward

Lewis

2020

Parasite Immunology

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Trypanosoma cruzi is a remarkably versatile parasite. It can parasitize almost any nucleated cell type and naturally infects hundreds of mammal species across much of the Americas. In humans, it is the cause of Chagas disease, a set of mainly chronic conditions predominantly affecting the heart and gastrointestinal tract, which can progress to become life threatening. Yet around two thirds of infected people are long‐term asymptomatic carriers. Clinical outcomes depend on many factors, but the central determinant is the nature of the host‐parasite interactions that play out over the years of chronic infection in diverse tissue environments. In this review, we aim to integrate recent developments in the understanding of the spatial and temporal dynamics of T. cruzi infections with established and emerging concepts in host immune responses in the corresponding phases and tissues.

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Section: Stage 2: Adaptive Responses Take Controlmentioning

confidence: 99%

Host‐parasite dynamics in Chagas disease from systemic to hyper‐local scales

Pérez‐Mazliah

Ward

Lewis

2020

Parasite Immunology

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“…Infection with Trypanosoma cruzi (T. cruzi), the etiological agent of Chagas disease, triggers both innate (1)(2)(3), and adaptive (4)(5)(6) immune responses that aim at the control of the parasite load both in tissues and peripheral blood [Reviewed in (7)]. However, these mechanisms do not succeed in the complete eradication of the parasite, which results in parasite persistence (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

IL-10-Dependent and -Independent Mechanisms Are Involved in the Cardiac Pathology Modulation Mediated by Fenofibrate in an Experimental Model of Chagas Heart Disease

et al. 2020

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“…The performances of both CD4 + and CD8 + T cell subpopulations have been observed during T. cruzi infection, irrespective of the route of infection studied (23,42,49). CD8 + T cells have been described as being of great importance for host resistance and effective control of the parasite outgrowth during acute and chronic infections (49,81,85). Studies indicate that CD8 + T lymphocytes fail to restrain parasitemia and tissue parasitism in the absence of CD4 + T cells (86).…”

Section: Discussionmentioning

confidence: 99%

Host Genetics Background Influence in the Intragastric Trypanosoma cruzi Infection

et al. 2020

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BackgroundConsidering the complexity of the factors involved in the immunopathology of Chagas disease, which influence the Chagas’ disease pathogenesis, anti-T. cruzi immune response, and chemotherapy outcome, further studies are needed to improve our understanding about these relationships. On this way, in this article we analyzed the host genetic influence on hematological, histopathological and immunological aspects after T. cruzi infection.MethodsBALB/c and A mice were intragastrically infected with T. cruzi SC2005 strain, isolated from a patient of an outbreak of Chagas disease. Parameters such as parasite load, survival rates, cytokines production, macrophages, T and B cell frequencies, and histopathology analysis were carried out.ResultsBALB/c mice presented higher parasitemia and mortality rates than A mice. Both mouse lineages exhibited hematological alterations suggestive of microcytic hypochromic anemia and histopathological alterations in stomach, heart and liver. The increase of CD8+ T cells, in heart, liver and blood, and the increase of CD19+ B cells, in liver, associated with a high level of proinflammatory cytokines (IL-6, TNF-α, IFN-γ), confer a resistance profile to the host. Although BALB/c animals exhibited the same findings observed in A mice, the response to infection occurred later, after a considerable parasitemia increase. By developing an early response to the infection, A mice were found to be less susceptible to T. cruzi SC2005 infection.ConclusionsHost genetics background shaping the response to infection. The early development of a cytotoxic cellular response profile with the production of proinflammatory cytokines is important to lead a less severe manifestation of Chagas disease.

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Understanding CD8+ T Cell Immunity to Trypanosoma cruzi and How to Improve It

Cited by 36 publications

References 110 publications

Host‐parasite dynamics in Chagas disease from systemic to hyper‐local scales

Host‐parasite dynamics in Chagas disease from systemic to hyper‐local scales

IL-10-Dependent and -Independent Mechanisms Are Involved in the Cardiac Pathology Modulation Mediated by Fenofibrate in an Experimental Model of Chagas Heart Disease

Host Genetics Background Influence in the Intragastric Trypanosoma cruzi Infection

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