ArticleMediators of inflammation2014
Myocardial gene expression of T-bet, GATA-3, Ror-γt, FoxP3, and hallmark cytokines in chronic Chagas disease cardiomyopathy: an essentially unopposed TH1-type response.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- SBC Guideline on the Diagnosis and Treatment of Patients with Cardiomyopathy of Chagas Disease - 2023.Arquivos brasileiros de cardiologia · 2023Guideline
- Association of IL18 genetic polymorphisms with Chagas disease in Latin American populations.PLoS neglected tropical diseases · 2019Pooled it
- A SpecificFrontiers in immunology · 2020Trial
- IL-33/ST2 Signaling Protects the Heart by Restraining Inflammation and Parasite Burden duringACS infectious diseases · 2026Article
- Single-Cell Targeted Transcriptomics Reveals Subset-Specific Immune Signatures Differentiating Asymptomatic and Cardiac Patients With Chronic Chagas Disease.The Journal of infectious diseases · 2025Article
- Sex Differences in Chagas Cardiomyopathy: a Comprehensive Review.Current heart failure reports · 2025Review
- Higher T-bet and IFN-γ expression in advanced chagasic megaesophagus indicates Th1 response in the chronic phase.Revista do Instituto de Medicina Tropical de Sao Paulo · 2025Article
- Cardiac and Digestive Forms of Chagas Disease: An Update on Pathogenesis, Genetics, and Therapeutic Targets.Mediators of inflammation · 2025Review
- Article
- Pirfenidone Prevents Heart Fibrosis during Chronic Chagas Disease Cardiomyopathy.International journal of molecular sciences · 2024Article
- Enteric nervous system regeneration and functional cure of experimental digestive Chagas disease with trypanocidal chemotherapy.Nature communications · 2024Article
- Cytokine Networks as Targets for Preventing and Controlling Chagas Heart Disease.Pathogens (Basel, Switzerland) · 2023Review
- Chagas Disease Megaesophagus Patients Carrying VariantBiomedicines · 2022Article
- Epigenetic regulation of transcription factor binding motifs promotes Th1 response in Chagas disease cardiomyopathy.Frontiers in immunology · 2022Article
- Modulation of Regulatory T Cells Activity by Distinct CD80 and CD86 Interactions With CD28/CTLA-4 in Chagas Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Rare Pathogenic Variants in Mitochondrial and Inflammation-Associated Genes May Lead to Inflammatory Cardiomyopathy in Chagas Disease.Journal of clinical immunology · 2021Article
- Physical Exercise Training and Chagas Disease: Potential Role of MicroRNAs.Arquivos brasileiros de cardiologia · 2021Review
- Host-parasite dynamics in Chagas disease from systemic to hyper-local scales.Parasite immunology · 2021Review
- The Blockade of Interleukin-2 During the Acute Phase ofFrontiers in cellular and infection microbiology · 2021Article
- Immunomodulation for the Treatment of Chronic Chagas Disease Cardiomyopathy: A New Approach to an Old Enemy.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic Chagas disease cardiomyopathy (CCC), a late consequence of Trypanosoma cruzi infection, is an inflammatory cardiomyopathy with prognosis worse than those of noninflammatory etiology (NIC). Although the T cell-rich myocarditis is known to play a pathogenetic role, the relative contribution of each of the functional T cell subsets has never been thoroughly investigated. We therefore assessed gene expression of cytokines and transcription factors involved in differentiation and effector function of each functional T cell subset (TH1/TH2/TH17/Treg) in CCC, NIC, and heart donor myocardial samples. METHODS AND
resultsQuantitative PCR showed markedly upregulated expression of IFN-γ and transcription factor T-bet, and minor increases of GATA-3; FoxP3 and CTLA-4; IL-17 and IL-18 in CCC as compared with NIC samples. Conversely, cytokines expressed by TH2 cells (IL-4, IL-5, and IL-13) or associated with Treg (TGF-β and IL-10) were not upregulated in CCC myocardium. Expression of TH1-related genes such as T-bet, IFN-γ, and IL-18 correlated with ventricular dilation, FoxP3, and CTLA-4.
conclusionsResults are consistent with a strong local TH1-mediated response in most samples, possibly associated with pathological myocardial remodeling, and a proportionally smaller FoxP3(+)CTLA4(+) Treg cell population, which is unable to completely curb IFN-γ production in CCC myocardium, therefore fueling inflammation.
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