Evidence map›Paper›PMID 36720995›Full record

ArticleScientific reports2023

Association of KIR2DL5, KIR2DS5, and KIR2DS1 allelic variation and atopic dermatitis.

David J Margolis, Nandita Mitra, Ole J Hoffstad, Ronald Berna, Brian S Kim, Abha Chopra, Elizabeth J Phillips

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Antiviral CD4Communications medicine · 2026
    Article
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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 2 countries.

David J MargolisDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, USA. margo@pennmedicine.upenn.edu.
Nandita MitraDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, USA.
Ole J HoffstadDepartment of Dermatology, Perelman School of Medicine, University of Pennsylvania, 901 Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104, USA.
Ronald BernaDepartment of Dermatology, Perelman School of Medicine, University of Pennsylvania, 901 Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104, USA.
Brian S KimDepartment of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Abha ChopraInstitute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Australia.
Elizabeth J PhillipsInstitute for Immunology and Infectious Diseases, Murdoch University, Murdoch, Australia.
Murdoch University · AUUniversity of Pennsylvania · USIcahn School of Medicine at Mount Sinai · US

Funding

Study Design and Data AnalysisP30AR069589 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI Elizabeth Anne Grice · 2016 to 2026
$8.6M
Skin Biology and Diseases Resource-based Center at Mount SinaiP30AR079200 · NIAMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Elena Ezhkova · 2021 to 2026
$5.2M
Atopic Dermatitis and High Resolution HLAR01AR070873 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MARGOLIS, DAVID, MONOS, DIMITRI S · 2017 to 2022
$2.4M
HIV modulation of BAG3 impacting quality control of Tau in neuronal cellsR01AG060962 · NIA · TEMPLE UNIV OF THE COMMONWEALTH · PI KHALILI, KAMEL · 2018 to 2022
$2.0M
NIAMS NIH HHS P30 AR069589NIAMS NIH HHS P30 AR079200NIAMS NIH HHS R01 AR070873NIA NIH HHS R01 AG060962
6 · The paper itself

Abstract

Natural killer cells (NK) have been associated with the pathophysiology of atopic dermatitis (AD). NK function is regulated by killer cell Ig-like receptor family (KIR) receptors that interact with HLA ligands. The study goal was to focus on allelic variation in genes KIR2DL5, KIR2DS5, and KIR2DS1 with respect to AD. This was a case-control study of individuals with (n = 313) and without (n = 176) AD. Associations were estimated using logistic regression. The prevalence of KIR2DL5 was 52.5% (95% CI 48.0,57.0), KIR2DS5 was 33.0% (28.8,37.3), and KIR2DS1 was 33.6% (29.4,38.0). The presence of the KIR2DL5*001:01 increased the odds of having AD by about 86% (odds ratio (OR): 1.86(1.23,2.82) p = 0.003). The risk for individuals homozygous for KIR2DL5*001:01 was even greater (OR: 2.16 (95% CI 1.31,3.53) p = 0.0023). The odds of having AD with KIR2DL5*001:01 was similar in Whites and Blacks. Allelic variation in KIR2DS5 and KIR2DS1 was not associated with AD. There is no known HLA binding ligand for KIR2DL5. The effect of KIR2DL5*001:01 increased in the presence of HLA-B*-21TT leader sequence (2.46(1.37,4.41) p = 0.0025) and the HLA-C2 ligand (2.07 (1.37,4.41, p = 0.000002). Our study shows an independent association of the KIR2DL5*001:01 with AD and is the first study to associate AD with KIR allelic variation.

Indexed as

Dermatitis, AtopicReceptors, KIRReceptors, KIR2DL5AllelesCase-Control StudiesGenes, MHC Class IHumansLigandsKIR2DS1 protein, humanKIR2DS5 protein, humanLigandsReceptors, KIRReceptors, KIR2DL5

Identifiers

PMID36720995
PMCPMC9889380
OpenAlexW4318616097

What Socratic holds

Textmetadata
LicenceCC BY
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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.