Evidence map›Paper›PMID 29323238›Full record

ArticleScientific reports2018

Human complement receptor type 1 (CR1) protein levels and genetic variants in chronic Chagas Disease.

Thaisa Lucas Sandri, Kárita Cláudia Freitas Lidani, Fabiana Antunes Andrade, Christian G Meyer, Peter G Kremsner, Iara J de Messias-Reason, Thirumalaisamy P Velavan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Application of Blood Group Genotyping by Next-Generation Sequencing in Various Immunohaematology Cases.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
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

7 authors at 3 institutions in 3 countries.

Thaisa Lucas SandriLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
Kárita Cláudia Freitas LidaniLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
Fabiana Antunes AndradeLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.ORCID http://orcid.org/0000-0003-4116-2324
Christian G MeyerInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Peter G KremsnerInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Iara J de Messias-ReasonLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
Thirumalaisamy P VelavanInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany. velavan@medizin.uni-tuebingen.de.
Universidade Federal do Paraná · BRDuy Tan University · VNUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement is an essential element in both innate and acquired immunity contributing to the immunopathogenesis of many disorders, including Chagas Disease (CD). Human complement receptor 1 (CR1) plays a role in the clearance of complement opsonized molecules and may facilitate the entry of pathogens into host cells. Distinct CR1 exon 29 variants have been found associated with CR1 expression levels, increased susceptibility and pathophysiology of several diseases. In this study, CR1 plasma levels were assessed by ELISA and CR1 variants in exon 29 by sequencing in a Brazilian cohort of 232 chronic CD patients and 104 healthy controls. CR1 levels were significantly decreased in CD patients compared to controls (p < 0.0001). The CR1 rs1704660G, rs17047661G and rs6691117G variants were significantly associated with CD and in high linkage disequilibrium. The CR1*AGAGTG haplotype was associated with T. cruzi infection (p = 0.035, OR 3.99, CI 1.1-14.15) whereas CR1*AGGGTG was related to the risk of chagasic cardiomyopathy (p = 0.028, OR 12.15, CI 1.13-113). This is the first study that provides insights on the role of CR1 in development and clinical presentation of chronic CD.

Indexed as

Polymorphism, Single NucleotideAdultAgedCase-Control StudiesChagas DiseaseFemaleHaplotypesHumansLinkage DisequilibriumMaleMiddle AgedReceptors, Complement 3bCR1 protein, humanReceptors, Complement 3b

Identifiers

PMID29323238
PMCPMC5765048
OpenAlexW2782254684

What OpenQuestion 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 OpenQuestion graph.