ArticlePloS one2013
Polymorphic sites at the immunoregulatory CTLA-4 gene are associated with chronic chagas disease and its clinical manifestations.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 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
- The Role of Immunogenetics in the Host-Parasite Interaction of Chagas Disease: Implications for Personalized Medicine.Tropical medicine and infectious disease · 2025Review
- Cardiac and Digestive Forms of Chagas Disease: An Update on Pathogenesis, Genetics, and Therapeutic Targets.Mediators of inflammation · 2025Review
- Cytokine Networks as Targets for Preventing and Controlling Chagas Heart Disease.Pathogens (Basel, Switzerland) · 2023Review
- Heart failure in cancer: role of checkpoint inhibitors.Journal of thoracic disease · 2018Review
- Review
- Innate immune receptors over expression correlate with chronic chagasic cardiomyopathy and digestive damage in patients.PLoS neglected tropical diseases · 2018Article
- The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease.Frontiers in immunology · 2018Review
- Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial.Memorias do Instituto Oswaldo Cruz · 2017Article
- Unconventional Pro-inflammatory CD4Frontiers in immunology · 2017Article
- Immunoregulatory mechanisms in Chagas disease: modulation of apoptosis in T-cell mediated immune responses.BMC infectious diseases · 2016Article
- Human leucocyte antigen-G (HLA-G) and its murine functional homolog Qa2 in the Trypanosoma cruzi Infection.Mediators of inflammation · 2015Article
- Chagas disease cardiomyopathy: immunopathology and genetics.Mediators of inflammation · 2014Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChagas disease affects approximately 10 million people mainly in Latin America. The immune regulation by the host seems to be an essential factor for disease evolution, and immune system inhibitory molecules such as CTLA-4 and PD-1 favor the maintenance of peripheral tolerance. Considering that polymorphisms at the immunoregulatory CTLA-4 and PDCD1 genes may alter their inhibitory function, we investigated the association of alleles, genotypes and haplotypes of polymorphic sites observed at the CTLA-4 and PDCD1 genes with different clinical manifestations of chronic Chagas disease (indeterminate, cardiac, digestive and mixed).
methodsThe polymorphisms at the CTLA-4 (-1722T/C, -318C/T and +49A/G) and PDCD1 (PD-1.3G/A) genes were typed using TaqMan methodology in 277 chronic Chagas disease patients classified into four groups, according to clinical characteristics, and 326 non-infected controls.
resultsOur results showed that CTLA-4 -1722CC genotype (22%), -1722C allele (27%) and CTLA-4 TCG (8.6%), TCA (26%) and CCA (15%) haplotypes were strongly associated with the indeterminate form, while the CTLA-4-318CT genotype (82%) and CTLA-4-318T allele (47%) were found mainly in patients with the mixed form of the disease. The CTLA-4 TCG haplotype (10.2%) was associated with the digestive form. On the other hand, the PD-1.3G/A polymorphism was not associated with chronic Chagas disease and its clinical manifestations.
conclusionsHere, we showed that alleles, genotypes and haplotypes reported to increase the expression of the regulatory molecule CTLA-4 were associated with the indeterminate form of the disease. Taken together, our data support the idea that polymorphic sites at immunoregulatory genes may influence the development of Chagas disease variants.
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