ArticleInfection and immunity2003
Evidence that development of severe cardiomyopathy in human Chagas' disease is due to a Th1-specific immune response.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 1 of them a synthesis that pooled it.
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Who cites it
143 citing papers in PubMed, 1 synthesis or guideline pooled it, 321 citations in OpenAlex.
- SBC Guideline on the Diagnosis and Treatment of Patients with Cardiomyopathy of Chagas Disease - 2023.Arquivos brasileiros de cardiologia · 2023Guideline
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- Trial
- IL-33/ST2 Signaling Sustains Hepato-Intestinal Homeostasis by Orchestrating Vascular Surveillance and Immune Regulatory Circuits During Experimental Trypanosoma cruzi Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Cytokine Profiles and Inflammatory Implications in Chagas Disease: Associations with Ventricular Function and Conduction Disorders.Medical sciences (Basel, Switzerland) · 2025Article
- Sex Differences in Chagas Cardiomyopathy: a Comprehensive Review.Current heart failure reports · 2025Review
- Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes.PLoS neglected tropical diseases · 2025Article
- The time has come for a vaccine against Chagas disease.Lancet regional health. Americas · 2025Review
- Therapeutical Potential and Immunomodulatory Profile ofACS infectious diseases · 2025Article
- Profile of soluble cell adhesion molecules as potential biomarkers in the cardiac stages of chronic Chagas disease.Frontiers in immunology · 2025Article
- Cardiac and Digestive Forms of Chagas Disease: An Update on Pathogenesis, Genetics, and Therapeutic Targets.Mediators of inflammation · 2025Review
- Mechanisms behind the high mortality rate in chronic Chagas cardiomyopathy: Unmasking a three-headed monster.European journal of heart failure · 2024Review
- Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection withPathogens (Basel, Switzerland) · 2024Article
- The Functions of Cytokines in the Cardiac Immunopathogenesis of Chagas Disease.Pathogens (Basel, Switzerland) · 2024Review
- Molecular similarities between the genes for Trypanosoma cruzi microtubule-associated proteins, mammalian interferons, and TRIMs.Parasitology research · 2024Article
- Vitamin D treatment distinctly modulates cytokine production by peripheral blood mononuclear cells among patients with chronic cardiac and indeterminate clinical forms of Chagas disease.Immunity, inflammation and disease · 2024Article
- Unraveling the Missing Pieces: Exploring the Gaps in Understanding Chagas Cardiomyopathy.Cureus · 2024Review
- Signatures of CD4Frontiers in immunology · 2024Article
- New insights intoFrontiers in immunology · 2024Review
83 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of interleukin 10 (IL-10) and gamma interferon (IFN-gamma) on the development of pathology in human Chagas' disease was investigated. Two categories of patients, low and high producers of IFN-gamma, were identified based on the levels of secretion of this cytokine in the supernatant of peripheral blood mononuclear cell (PBMC) cultures. Eighty-three percent of the patients presenting with cardiac disease (CARD) of different degrees and 59% of the patients with the indeterminate form of disease (IND) were identified as high IFN-gamma producers. PBMC from IND patients classified as low IFN-gamma producers secreted significantly higher amounts of IL-10 than did those from other groups. Flow cytometry analysis demonstrated that in PBMC from the IND group, the majority of the IL-10-producing cells were monocytes (CD14(High+) cells), whereas in the CARD group, the major sources of IFN-gamma were T lymphocytes (CD3(+) CD4(+) cells). These results suggest an association between the production of IFN-gamma by CD3(+) CD4(+) cells and morbidity in Chagas' disease, whereas the production of IL-10 by macrophages/monocytes leads to regulation of the immune response in IND patients. We hypothesize that an exacerbated production of IFN-gamma against Trypanosoma cruzi antigens favors the development of a strong Th1 response in CARD patients, which leads to progression of heart disease.
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