Evidence map›Paper›PMID 33875297›Full record

ArticleHuman immunology2021

Human leukocyte antigen class-I variation is associated with atopic dermatitis: A case-control study.

D J Margolis, N Mitra, J L Duke, R Berna, J D Margolis, O Hoffstad, B S Kim, A C Yan, A L Zaenglein, Z Chiesa Fuxench and 8 more

Open access · greenAbstract read
In one paragraph

Article in Human immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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  10. Association of KIR Genes and MHC Class I Ligands with Atopic Dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    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

18 authors at 3 institutions in 1 country.

D J MargolisDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, United States; Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States. Electronic address: margo@pennmedicine.upenn.edu.
N MitraDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, United States.
J L DukeDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
R BernaDepartment of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
J D MargolisDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, United States.
O HoffstadDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, United States.
B S KimDivision of Dermatology, Department of Medicine, Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, United States.
A C YanDivision of Dermatology, Department of Medicine, Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, United States.
A L ZaengleinDepartments of Dermatology and Pediatrics, Pennsylvania State University/Hershey Medical Center, Hershey, PA, United States.
Z Chiesa FuxenchDepartment of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
A DinouDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
J WassermanDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
N TairisDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
T L MosbrugerDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
D FerriolaDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
Georgios DamianosDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
Ioanna KotsopoulouDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
D S MonosDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, United States; Department of Pathology and Laboratory Medicine, Perelman Schools of Medicine, University of Pennsylvania, Philadelphia, PA, United States. Electronic address: monosd@email.chop.edu.
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · USPennsylvania State University · US

Funding

Atopic Dermatitis and High Resolution HLAR01AR070873 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MARGOLIS, DAVID, MONOS, DIMITRI S · 2017 to 2022
$2.4M
African-Americans with Atopic Dermatitis: Skin Barrier and ImmuneR01AR069062 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MARGOLIS, DAVID · 2016 to 2021
$2.4M
NIAMS NIH HHS R01 AR069062NIAMS NIH HHS R01 AR070873
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a common immune-medicated skin disease. Previous studies have explored the relationship between Human Leukocyte Antigen (HLA) allelic variation and AD with conflicting results. The aim was to examine HLA Class I genetic variation, specifically peptide binding groove variation, and associations with AD. A case-control study was designed to evaluate HLA class I allelic variation and binding pocket polymorphisms, using next generation sequencing on 464 subjects with AD and 388 without AD. Logistic regression was used to evaluate associations with AD by estimating odds ratios (95% confidence intervals). Significant associations were noted with susceptibility to AD (B*53:01) and protection from AD (A*01:01, A*02:01, B*07:02 and C*07:02). Evaluation of polymorphic residues in Class I binding pockets revealed six amino acid residues conferring protection against AD: A9F (HLA-A, position 9, phenylalanine) [pocket B/C], A97I [pocket C/E], A152V [pocket E], A156R [pocket D/E], B163E [pocket A] and C116S [pocket F]. These findings demonstrate that specific HLA class I components are associated with susceptibility or protection from AD. Individual amino acid residues are relevant to protection from AD and set the foundation for evaluating potential HLA Class I molecules in complex with peptides/antigens that may initiate or interfere with T-cell responses.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationAllelesCase-Control StudiesDermatitis, AtopicGene FrequencyGenetic Association StudiesGenotypeHistocompatibility Antigens Class IHumansModels, MolecularOdds RatioPolymorphism, Single NucleotideProtein ConformationSequence Analysis, DNAStructure-Activity RelationshipHistocompatibility Antigens Class IAllergyAtopic dermatitisCase-control studyHuman leukocyte antigen

Identifiers

PMID33875297
PMCPMC8238855
OpenAlexW3155940419

What OpenQuestion holds

Textmetadata
LicenceTDM
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.