Evidence map›Paper›PMID 21734249›Full record

ReviewClinical microbiology reviews2011

Pathogenesis of chagas' disease: parasite persistence and autoimmunity.

Antonio R L Teixeira, Mariana M Hecht, Maria C Guimaro, Alessandro O Sousa, Nadjar Nitz

Open access · greenAbstract readReview
In one paragraph

Review in Clinical microbiology reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

103 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pharmacological interventions for treating heart failure in patients with Chagas cardiomyopathy.The Cochrane database of systematic reviews · 2016 · on this map
    Pooled it
  2. Article
  3. Chagas disease: host responses, parasite evasion and vaccine advances.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2026
    Review
  4. Article
  5. Clinical Progression of Cardiac ChronicPathogens (Basel, Switzerland) · 2025
    Article
  6. Article
  7. BeyondInternational journal of molecular sciences · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Effects of Free and Nanoencapsulated Benznidazole in AcutePharmaceuticals (Basel, Switzerland) · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

43 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Antonio R L TeixeiraChagas Disease Multidisciplinary Research Laboratory, University of Brasilia, Federal District, Brazil. ateixeir@unb.br
Mariana M Hecht
Maria C Guimaro
Alessandro O Sousa
Nadjar Nitz
Universidade de Brasília · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute Trypanosoma cruzi infections can be asymptomatic, but chronically infected individuals can die of Chagas' disease. The transfer of the parasite mitochondrial kinetoplast DNA (kDNA) minicircle to the genome of chagasic patients can explain the pathogenesis of the disease; in cases of Chagas' disease with evident cardiomyopathy, the kDNA minicircles integrate mainly into retrotransposons at several chromosomes, but the minicircles are also detected in coding regions of genes that regulate cell growth, differentiation, and immune responses. An accurate evaluation of the role played by the genotype alterations in the autoimmune rejection of self-tissues in Chagas' disease is achieved with the cross-kingdom chicken model system, which is refractory to T. cruzi infections. The inoculation of T. cruzi into embryonated eggs prior to incubation generates parasite-free chicks, which retain the kDNA minicircle sequence mainly in the macrochromosome coding genes. Crossbreeding transfers the kDNA mutations to the chicken progeny. The kDNA-mutated chickens develop severe cardiomyopathy in adult life and die of heart failure. The phenotyping of the lesions revealed that cytotoxic CD45, CD8(+) γδ, and CD8α(+) T lymphocytes carry out the rejection of the chicken heart. These results suggest that the inflammatory cardiomyopathy of Chagas' disease is a genetically driven autoimmune disease.

Indexed as

AnimalsAutoimmunityChagas DiseaseChickensDisease Models, AnimalHumansTrypanosoma cruzi

Identifiers

PMID21734249
PMCPMC3131057
OpenAlexW2157744996

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.