ArticleBMC infectious diseases2016
Immunoregulatory mechanisms in Chagas disease: modulation of apoptosis in T-cell mediated immune responses.
Article in BMC infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Risk Factors for Progression to Chronic Chagas Cardiomyopathy: A Systematic Review and Meta-Analysis.The American journal of tropical medicine and hygiene · 2023Pooled it
- Omega-3 supplementation on inflammatory markers in patients with chronic Chagas cardiomyopathy: a randomized clinical study.Nutrition journal · 2017Trial
- Review
- Apoptosis: A Key Process ThatJournal of parasitology research · 2025Review
- Cardiac involvement in Chagas disease and African trypanosomiasis.Nature reviews. Cardiology · 2024Review
- Immunopathogenesis inFrontiers in immunology · 2023Review
- Modulation of Regulatory T Cells Activity by Distinct CD80 and CD86 Interactions With CD28/CTLA-4 in Chagas Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Physical Exercise Promotes a Reduction in Cardiac Fibrosis in the Chronic Indeterminate Form of Experimental Chagas Disease.Frontiers in immunology · 2021Article
- Innate Immune Sensing by Cells of the Adaptive Immune System.Frontiers in immunology · 2020Review
- Co-infection with distinct Trypanosoma cruzi strains induces an activated immune response in human monocytes.Parasite immunology · 2019Article
- A retrospective study on the influence of siblings' relatedness in Bolivian patients with chronic Chagas disease.Parasites & vectors · 2019Article
- Review
- Implication of Apoptosis for the Pathogenesis ofFrontiers in immunology · 2017Review
- Efferocytosis of Pathogen-Infected Cells.Frontiers in immunology · 2017Review
- Distinct Trypanosoma cruzi isolates induce activation and apoptosis of human neutrophils.PloS one · 2017Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic Chagas disease presents different clinical manifestations ranging from asymptomatic (namely indeterminate) to severe cardiac and/or digestive. Previous results have shown that the immune response plays an important role, although no all mechanisms are understood. Immunoregulatory mechanisms such as apoptosis are important for the control of Chagas disease, possibly affecting the morbidity in chronic clinical forms. Apoptosis has been suggested to be an important mechanism of cellular response during T. cruzi infection. We aimed to further understand the putative role of apoptosis in Chagas disease and its relation to the clinical forms of the disease.
methodsApoptosis of lymphocytes, under antigenic stimuli (soluble T. cruzi antigens - TcAg) where compared to that of non-stimulated cells. Apoptosis was evaluated using the expression of annexin and caspase 3(+) by T cells and the percentage of cells positive evaluated by flow cytometry. In addition activation and T cell markers were used for the identification of TCD4(+) and TCD8(+) subpopulations. The presence of intracellular and plasma cytokines were also evaluated. Analysis of the activation status of the peripheral blood cells showed that patients with Chagas disease presented higher levels of activation determined by the expression of activation markers, after TcAg stimulation. PCR array were used to evaluate the contribution of this mechanism in specific cell populations from patients with different clinical forms of human Chagas disease.
resultsOur results showed a reduced proliferative response associated a high expression of T CD4(+)CD62L(-) cells in CARD patients when compared with IND group and NI individuals. We also observed that both groups of patients presented a significant increase of CD4(+) and CD8(+) T cell subsets in undergoing apoptosis after in vitro stimulation with T. cruzi antigens. In CARD patients, both CD4(+) and CD8(+) T cells expressing TNF-α were highly susceptible to undergo apoptosis after in vitro stimulation. Interestingly, the in vitro TcAg stimulation increased considerably the expression of cell death TNF/TNFR superfamily and Caspase family receptors genes in CARD patients.
conclusionsTaken together, our results suggest that apoptosis may be an important mechanism for the control of morbidity in T. cruzi infection by modulating the expression of apoptosis genes, the cytokine environment and/or killing of effector cells.
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