ArticleInfection and immunity2007
Modulation of autoimmunity by treatment of an infectious disease.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Endothelial transmigration by Trypanosoma cruzi.PloS one · 2013Trial
- Diagnosing Chagas in Pregnancy and Childhood: What's Old and New.Clinics in laboratory medicine · 2025Review
- Self and parasite-derived peptides selected upon DERAA-bearing HLA-DRB1 alleles activate CD4+ T cells from Chagas cardiomyopathy patients and are associated with ventricular dysfunction.Frontiers in immunology · 2025Article
- Unraveling the Missing Pieces: Exploring the Gaps in Understanding Chagas Cardiomyopathy.Cureus · 2024Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- Signal Transducer and Activator of Transcription-3 Modulation of Cardiac Pathology in Chronic Chagasic Cardiomyopathy.Frontiers in cellular and infection microbiology · 2021Article
- Nano-Medicines a Hope for Chagas Disease!Frontiers in molecular biosciences · 2021Review
- Precision Health for Chagas Disease: Integrating Parasite and Host Factors to Predict Outcome of Infection and Response to Therapy.Frontiers in cellular and infection microbiology · 2020Review
- Low-Level Parasite Persistence Drives Vasculitis and Myositis in Skeletal Muscle of Mice Chronically Infected with Trypanosoma cruzi.Infection and immunity · 2019Article
- Pathology and Pathogenesis of Chagas Heart Disease.Annual review of pathology · 2019Review
- Advances in nanocarriers as drug delivery systems in Chagas disease.International journal of nanomedicine · 2019Review
- Putting Infection Dynamics at the Heart of Chagas Disease.Trends in parasitology · 2016Review
- Host and parasite genetics shape a link between Trypanosoma cruzi infection dynamics and chronic cardiomyopathy.Cellular microbiology · 2016Article
- Curcumin Enhances the Anti-Trypanosoma cruzi Activity of Benznidazole-Based Chemotherapy in Acute Experimental Chagas Disease.Antimicrobial agents and chemotherapy · 2016Article
- Autoimmune pathogenesis of Chagas heart disease: looking back, looking ahead.The American journal of pathology · 2015Review
- Depletion of regulatory T cells decreases cardiac parasitosis and inflammation in experimental Chagas disease.Parasitology research · 2015Article
- Towards a paradigm shift in the treatment of chronic Chagas disease.Antimicrobial agents and chemotherapy · 2014Article
- Mechanisms of Trypanosoma cruzi persistence in Chagas disease.Cellular microbiology · 2012Review
- Pathogenesis of Chagas disease: time to move on.Frontiers in bioscience (Elite edition) · 2012Article
- Advances and challenges towards a vaccine against Chagas disease.Human vaccines · 2011Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Chagas' heart disease (CHD), caused by the parasite Trypanosoma cruzi, is the most common form of myocarditis in Central America and South America. Some humans and experimental animals develop both humoral and cell-mediated cardiac-specific autoimmunity during infection. Benznidazole, a trypanocidal drug, is effective at reducing parasite load and decreasing the severity of myocarditis in acutely infected patients. We hypothesized that the magnitude of autoimmunity that develops following T. cruzi infection is directly proportional to the amount of damage caused by the parasite. To test this hypothesis, we used benznidazole to reduce the number of parasites in an experimental model of CHD and determined whether this treatment altered the autoimmune response. Infection of A/J mice with the Brazil strain of T. cruzi leads to the development of severe inflammation, fibrosis, necrosis, and parasitosis in the heart accompanied by vigorous cardiac myosin-specific delayed-type hypersensitivity (DTH) and antibody production at 21 days postinfection. Mice succumbed to infection within a month if left untreated. Treatment of infected mice with benznidazole eliminated mortality and decreased disease severity. Treatment also reduced cardiac myosin-specific DTH and antibody production. Reinfection of treated mice with a heart-derived, virulent strain of T. cruzi or immunization with myosin led to the redevelopment of myosin-specific autoimmune responses and inflammation. These results provide a direct link between the levels of T. cruzi and the presence of autoimmunity and suggest that elimination of the parasite may result in the reduction or elimination of autoimmunity in the chronic phase of infection.
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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.