Evidence map›Paper›PMID 28801811›Full record

ArticleClinical rheumatology2017

Association of variably expressed KIR3dl1 alleles with psoriatic disease.

Jeffrey Berinstein, Remy Pollock, Fawnda Pellett, Arane Thavaneswaran, Vinod Chandran, Dafna D Gladman

Abstract read
PubMed Publisher
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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Current research status of HLA in immune-related diseases.Immunity, inflammation and disease · 2021
    Review
  5. Rheumatoid Arthritis Susceptibility Is Associated with theReports of biochemistry & molecular biology · 2021
    Article
  6. Article
  7. The Genetics of Spondyloarthritis.Journal of personalized medicine · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. 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

6 authors at 1 institution in 2 countries.

Jeffrey BerinsteinUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Remy PollockUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Fawnda PellettUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Arane ThavaneswaranUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Vinod ChandranUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Dafna D GladmanUniversity of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases 1E-410B, Toronto Western Hospital, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada. dafna.gladman@utoronto.ca.ORCID http://orcid.org/0000-0002-9074-0592
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this study is to examine the genetic interaction of variably expressed killer cell immunoglobulin-like receptor (KIR) 3DL1 alleles with their cognate ligand, human leukocyte antigen (HLA)-Bw4, in susceptibility to psoriatic disease (PsD). A novel allelic typing system was developed to differentiate KIR3DL1 alleles (*High, *Low, *Null expression, and 3DS1), in PsD patients, including those with psoriatic arthritis (PsA) and cutaneous psoriasis without arthritis (PsC) and healthy controls. Frequencies of each KIR3DL1 allele, Bw4-80I and Bw4-80T, as well as the genetic interaction between the KIR3DL1 alleles and the Bw4 epitope were analyzed. KIR3DL1 alleles were successfully genotyped in 392 PsA, 260 PsC, and 371 control subjects. Only the KIR3DL1*Null allele was associated with PsD (OR = 0.69, p = 0.008), both in the PsA (OR = 0.69, p = 0.02) and PsC patients (OR = 0.70, p = 0.04) compared to control subjects. No difference in the frequency of KIR3DL1*Null was found between the PsA and PsC patients. The presence of the HLA-Bw4 epitope was significantly associated with PsD, particularly in the PsA patients compared to controls. Bw4-80I was increased in PsD and PsA subjects, but not in PsC patients compared to controls. Bw4-80T was increased in PsA compared to both PsC patients or to controls. No interaction was detected between any of the KIR3DL1 alleles and HLA-Bw4, Bw4-80I, or Bw4-80T. The novel qPCR technique successfully identified the four variably expressed KIR3DL1 alleles. The HLA-Bw4 epitope was associated with psoriatic disease, particularly with PsA, but no genetic interactions with KIR3DL1 alleles were detected.

Indexed as

Genetic Predisposition to DiseaseAdultAllelesArthritis, PsoriaticCase-Control StudiesEpitopesFemaleGenotypeHLA AntigensHLA-B AntigensHumansInflammationMaleMiddle AgedPolymerase Chain ReactionReceptors, KIR3DL1EpitopesHLA AntigensHLA-B AntigensHLA-Bw4 antigenKIR3DL1 protein, humanReceptors, KIR3DL1KIRKIR3DL1PsoriasisPsoriatic arthritisPsoriatic disease

Identifiers

PMID28801811
OpenAlexW2744217149

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.