Evidence map›Paper›PMID 31122742›Full record

ArticleHuman immunology2019

HLA-C variants associated with amino acid substitutions in the peptide binding groove influence susceptibility to Kawasaki disease.

Chisato Shimizu, Jihoon Kim, Hariklia Eleftherohorinou, Victoria J Wright, Long T Hoang, Adriana H Tremoulet, Alessandra Franco, Martin L Hibberd, Atsushi Takahashi, Michiaki Kubo and 8 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Immunogenetics of Kawasaki disease.Clinical reviews in allergy & immunology · 2020
    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

18 authors at 9 institutions in 5 countries.

Chisato ShimizuDepartment of Pediatrics, University California San Diego, La Jolla, CA, USA. Electronic address: c1shimizu@ucsd.edu.
Jihoon KimDivision of Biomedical Informatics, Department of Medicine, University California San Diego, La Jolla, CA, USA.
Hariklia EleftherohorinouSection of Paediatrics, Division of Infectious Diseases, Department of Medicine, Imperial College London, London, UK.
Victoria J WrightSection of Paediatrics, Division of Infectious Diseases, Department of Medicine, Imperial College London, London, UK.
Long T HoangGenome Institute of Singapore, Singapore.
Adriana H TremouletDepartment of Pediatrics, University California San Diego, La Jolla, CA, USA; Department of Cardiology, Rady Childrens' Hospital San Diego, San Diego, CA, USA.
Alessandra FrancoDepartment of Pediatrics, University California San Diego, La Jolla, CA, USA.
Martin L HibberdGenome Institute of Singapore, Singapore.
Atsushi TakahashiLaboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan; Department of Genomic Medicine, Research Institute, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Michiaki KuboRIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan.
Kaoru ItoLaboratory for Cardiovascular Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan.
Toshihiro TanakaDepartment of Human Genetics and Disease Diversity, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Bunkyo-ku, Tokyo, Japan.
Yoshihiro OnouchiLaboratory for Cardiovascular Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan; Department of Public Health, Chiba University Graduate School of Medicine, Chiba, Japan.
Lachlan J M CoinInstitute for Molecular Bioscience, University of Queensland, St Lucia, Australia.
Michael LevinSection of Paediatrics, Division of Infectious Diseases, Department of Medicine, Imperial College London, London, UK.
Jane C BurnsDepartment of Pediatrics, University California San Diego, La Jolla, CA, USA; Department of Cardiology, Rady Childrens' Hospital San Diego, San Diego, CA, USA.
Hiroko ShikeDepartment of Pathology, HLA Laboratory, Penn State Hershey Medical Center, Hershey, PA, USA.
International Kawasaki Disease Genetic Consortium
University of California San Diego · USImperial College London · GBGenome Institute of Singapore · SGRIKEN Center for Integrative Medical Sciences · JPChiba University · JPNational Cerebral and Cardiovascular Center · JPPenn State Milton S. Hershey Medical Center · USThe University of Queensland · AUTokyo Medical and Dental University · JP

Funding

iDASH: Integrating Data for Analysis, Anonymization, and SharingU54HL108460 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OHNO-MACHADO, LUCILA · 2010 to 2015
$19.1M
Genetic Markers and gene expression in Kawasaki DiseaseR01HL069413 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BURNS, JANE C · 2002 to 2010
$5.5M
NHLBI NIH HHS R01 HL069413NHLBI NIH HHS U54 HL108460
6 · The paper itself

Abstract

Kawasaki disease (KD) is a pediatric vasculitis caused by an unknown trigger in genetically susceptible children. The incidence varies widely across genetically diverse populations. Several associations with HLA Class I alleles have been reported in single cohort studies. Using a genetic approach, from the nine single nucleotide variants (SNVs) associated with KD susceptibility in children of European descent, we identified SNVs near the HLA-C (rs6906846) and HLA-B genes (rs2254556) whose association was replicated in a Japanese descent cohort (rs6906846 p = 0.01, rs2254556 p = 0.005). The risk allele (A at rs6906846) was also associated with HLA-C*07:02 and HLA-C*04:01 in both US multi-ethnic and Japanese cohorts and HLA-C*12:02 only in the Japanese cohort. The risk A-allele was associated with eight non-conservative amino acid substitutions (amino acid positions); Asp or Ser (9), Arg (14), Ala (49), Ala (73), Ala (90), Arg (97), Phe or Ser (99), and Phe or Ser (116) in the HLA-C peptide binding groove that binds peptides for presentation to cytotoxic T cells (CTL). This raises the possibility of increased affinity to a "KD peptide" that contributes to the vasculitis of KD in genetically susceptible children.

Indexed as

Genetic Predisposition to DiseaseAllelesAmino Acid SequenceAmino Acid SubstitutionAntigen PresentationBinding SitesCohort StudiesGene FrequencyGenotypeHistocompatibility TestingHLA-C AntigensHumansJapanMucocutaneous Lymph Node SyndromePeptidesPolymorphism, Single NucleotideHLA-C AntigensPeptidesAmino acid substitutionAntigen presentationCytotoxic T cellsHLA-CKawasaki disease

Identifiers

PMID31122742
PMCPMC10793643
OpenAlexW2945622661

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.