Evidence map›Paper›PMID 27988812›Full record

ArticleClinical rheumatology2017

CD28, CTLA-4 and CCL5 gene polymorphisms in patients with rheumatoid arthritis.

Katarzyna Luterek-Puszyńska, Damian Malinowski, Agnieszka Paradowska-Gorycka, Krzysztof Safranow, Andrzej Pawlik

Abstract read
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In one paragraph

Article in Clinical rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Association betweenAging · 2021
    Pooled it
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  13. The Association BetweenFrontiers in medicine · 2021
    Article
  14. Association of the genetic polymorphisms in inhibiting and activating molecules of immune system with rheumatoid arthritis: A systematic review and meta-analysis.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021
    Review
  15. Article
  16. Article
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  19. Article
  20. Bioinformatics Analysis and Identification of Genes and Molecular Pathways Involved in Synovial Inflammation in Rheumatoid Arthritis.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
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 2 institutions in 1 country.

Katarzyna Luterek-PuszyńskaDepartment of Physiology, Pomeranian Medical University, Powstancow Wlkp. 72, 70-111, Szczecin, Poland.
Damian MalinowskiDepartment of Physiology, Pomeranian Medical University, Powstancow Wlkp. 72, 70-111, Szczecin, Poland.
Agnieszka Paradowska-GoryckaDepartment of Biochemistry and Molecular Biology, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.
Krzysztof SafranowDepartment of Biochemistry and Medical Chemistry, Pomeranian Medical University, Szczecin, Poland.
Andrzej PawlikDepartment of Physiology, Pomeranian Medical University, Powstancow Wlkp. 72, 70-111, Szczecin, Poland. pawand@poczta.onet.pl.
Pomeranian Medical University · PLNational Institute of Geriatrics, Rheumatology and Rehabilitation · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint destruction caused by infiltrating leukocytes including T cells. An important role in T cell co-stimulation is played by the CD28, as a stimulatory signal transducer and the inhibitory CTLA-4. CCL5 is produced by circulating T cells and plays an active role in the chemotactic activity of T cells in RA. The aim of this study was to examine the associations between polymorphisms within CD28, CTLA-4, and CCL5 genes and RA. We examined 422 patients (340 female, 82 male, mean age 57.5 ± 12.5 years) with rheumatoid arthritis and 338 healthy subjects (261 female, 77 male). Disease activity was determined on the basis of DAS28 score. The patients with DAS28 of ≤2.5 were classified as subjects in remission of disease symptoms; the patients who had DAS28 of >2.5 were classified as subjects with active form of RA. There were no statistically significant differences in the distribution of studied genotypes and alleles between RA patients and the control group. A statistically significant difference was observed in the distribution of CTLA4 exon 1 +49A>G rs231775 genotypes between patients with DAS28 ≤ 2.5 and DAS28 > 2.5 where the increased frequency of AA genotype among patients with DAS28 > 2.5 was revealed (OR 1.55; 95% CI 1.01-2.38). The results of our study suggest no significant association between CD28 rs1980422, CCL5 rs2107538, CTLA-4 exon 1 +49A>G rs231775 and rs3087243 gene polymorphisms and RA in the Polish population. Our results indicate a possible association between CTLA-4 exon 1 +49A>G rs231775 gene polymorphism and RA activity.

Indexed as

Polymorphism, Single NucleotideAllelesArthritis, RheumatoidCD28 AntigensCTLA-4 AntigenDNAFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHaplotypesHumansIncidenceMaleMiddle AgedPolandCD28 AntigensCTLA-4 AntigenCTLA4 protein, humanDNACCL5CD28CTLA-4PolymorphismRheumatoid arthritis

Identifiers

PMID27988812
OpenAlexW2565345863

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Registered trials

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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.