ArticlePloS one2011
Heat-killed Trypanosoma cruzi induces acute cardiac damage and polyantigenic autoimmunity.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Endothelial transmigration by Trypanosoma cruzi.PloS one · 2013Trial
- Review
- Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes.PLoS neglected tropical diseases · 2025Article
- Cardiac involvement in Chagas disease and African trypanosomiasis.Nature reviews. Cardiology · 2024Review
- Chronic Chagas Disease-the Potential Role of Reinfections in Cardiomyopathy Pathogenesis.Current heart failure reports · 2022Review
- Leishmaniasis and Chagas disease: Is there hope in nanotechnology to fight neglected tropical diseases?Frontiers in cellular and infection microbiology · 2022Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Shared neuroimmune and oxidative pathways underpinning Chagas disease and major depressive disorder.Translational psychiatry · 2020Review
- Pathology and Pathogenesis of Chagas Heart Disease.Annual review of pathology · 2019Review
- Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi.Infection and immunity · 2016Article
- Vaccination of dogs with Trypanosoma rangeli induces antibodies against Trypanosoma cruzi in a rural area of Córdoba, Argentina.Memorias do Instituto Oswaldo Cruz · 2016Article
- Autoimmune pathogenesis of Chagas heart disease: looking back, looking ahead.The American journal of pathology · 2015Review
- Three-dimensional structures in the design of therapeutics targeting parasitic protozoa: reflections on the past, present and future.Acta crystallographica. Section F, Structural biology communications · 2015Review
- Depletion of regulatory T cells decreases cardiac parasitosis and inflammation in experimental Chagas disease.Parasitology research · 2015Article
- Trypanosoma cruzi and Its Soluble Antigens Induce NET Release by Stimulating Toll-Like Receptors.PloS one · 2015Article
- Inhibition of autoimmune Chagas-like heart disease by bone marrow transplantation.PLoS neglected tropical diseases · 2014Article
- Immunopathologic characterization of naturally acquired Trypanosoma cruzi infection and cardiac sequalae in cynomolgus macaques (Macaca fascicularis).Journal of the American Association for Laboratory Animal Science : JAALAS · 2013Article
- Modulation of immune response in experimental Chagas disease.World journal of experimental medicine · 2013Review
- Parasite induced genetically driven autoimmune Chagas heart disease in the chicken model.Journal of visualized experiments : JoVE · 2012Article
- Pathogenesis of Chagas disease: time to move on.Frontiers in bioscience (Elite edition) · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Chagas heart disease, caused by the protozoan parasite Trypanosoma cruzi, is a potentially fatal cardiomyopathy often associated with cardiac autoimmunity. T. cruzi infection induces the development of autoimmunity to a number of antigens via molecular mimicry and other mechanisms, but the genesis and pathogenic potential of this autoimmune response has not been fully elucidated. To determine whether exposure to T. cruzi antigens alone in the absence of active infection is sufficient to induce autoimmunity, we immunized A/J mice with heat-killed T. cruzi (HKTC) emulsified in complete Freund's adjuvant, and compared the resulting immune response to that induced by infection with live T. cruzi. We found that HKTC immunization is capable of inducing acute cardiac damage, as evidenced by elevated serum cardiac troponin I, and that this damage is associated with the generation of polyantigenic humoral and cell-mediated autoimmunity with similar antigen specificity to that induced by infection with T. cruzi. However, while significant and preferential production of Th1 and Th17-associated cytokines, accompanied by myocarditis, develops in T. cruzi-infected mice, HKTC-immunized mice produce lower levels of these cytokines, do not develop Th1-skewed immunity, and lack tissue inflammation. These results demonstrate that exposure to parasite antigen alone is sufficient to induce autoimmunity and cardiac damage, yet additional immune factors, including a dominant Th1/Th17 immune response, are likely required to induce cardiac inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.