Evidence map›Paper›PMID 26658904›Full record

ArticlePloS one2015

Association of Killer Cell Immunoglobulin- Like Receptor Genes in Iranian Patients with Rheumatoid Arthritis.

Masoumeh Nazari, Mahdi Mahmoudi, Farzaneh Rahmani, Masoomeh Akhlaghi, Maani Beigy, Maryam Azarian, Elmira Shamsian, Maryam Akhtari, Reza Mansouri

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The role of NK cells in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  5. Rheumatoid Arthritis Susceptibility Is Associated with theReports of biochemistry & molecular biology · 2021
    Article
  6. Association ofJournal of diabetes and metabolic disorders · 2020
    Review
  7. Article
  8. Article
  9. 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

9 authors at 3 institutions in 1 country.

Masoumeh NazariImmunology Department, Shahid Sadoughi University of Medical Sciences (International Campus), Yazd, Iran.
Mahdi MahmoudiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Farzaneh RahmaniRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Masoomeh AkhlaghiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Maani BeigyRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Maryam AzarianRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Elmira ShamsianRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Maryam AkhtariRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Reza MansouriImmunology Department, Shahid Sadoughi University of Medical Sciences (International Campus), Yazd, Iran.
Tehran University of Medical Sciences · IRShariati Hospital · IRShahid Sadoughi University of Medical Sciences and Health Services · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by persistent synovitis, ultimately leading to cartilage and bone degeneration. Natural Killer cells and CD28 null T-cells are suspected as role players in RA pathogenesis. These cells are similar in feature and function, as they both exert their cytotoxic effect via Killer Cell Immunoglobulin- Like Receptors (KIR) on their surface. KIR genes have either an inhibitory or activating effect depending on their intracytoplasmic structure. Herein we genotyped 16 KIR genes, 3 pseudo genes and 6 HLA class І genes as their corresponding ligands in RA patients and control subjects.

methodsIn this case-control study, KIR and HLA genes were genotyped in 400 RA patients and 372 matched healthy controls using sequence-specific primers (SSP-PCR). Differences in the frequency of genes and haplotypes were determined by χ² test.

resultsKIR2DL2, 2DL5a, 2DL5b and activating KIR: KIR2DS5 and 3DS1 were all protective against RA. KIR2DL5 removal from a full Inhibitory KIR haplotype converted the mild protection (OR = 0.56) to a powerful predisposition to RA (OR = 16.47). Inhibitory haplotype No. 7 comprising KIR2DL5 in the absence of KIR2DL1 and KIR2DL3 confers a 14-fold protective effect against RA.

conclusionIndividuals carrying the inhibitory KIR haplotype No. 6 have a high potential risk for developing RA.

Indexed as

Genetic Predisposition to DiseaseAdultAgedArthritis, RheumatoidCase-Control StudiesDisease ResistanceFemaleGene ExpressionHaplotypesHLA-C AntigensHumansKiller Cells, NaturalMaleMiddle AgedMolecular TypingPseudogenesHLA-C AntigensReceptors, KIR

Identifiers

PMID26658904
PMCPMC4687638
OpenAlexW2216203345

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.