Evidence map›Paper›PMID 25809546›Full record

ArticleInternational journal of immunogenetics2015

Imputation of class I and II HLA loci using high-density SNPs from ImmunoChip and their associations with Kawasaki disease in family-based study.

S Shrestha, H W Wiener, B Aissani, A Shendre, J Tang, M A Portman

Abstract read
In one paragraph

Article in International journal of immunogenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. [Research advances in the pathogenesis of familial Kawasaki disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

6 authors at 2 institutions in 1 country.

S ShresthaDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
H W WienerDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
B AissaniDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
A ShendreDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
J TangDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
M A PortmanDepartment of Pediatrics, University of Washington, Seattle Children's Research Institute, Seattle, WA, USA.
University of Alabama at Birmingham · USUniversity of Washington · US

Funding

FcR Mutations in Kawasaki DiseaseR21HL090558 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI PORTMAN, MICHAEL A · 2007 to 2008
$466k
NHLBI NIH HHS R21 HL090558
6 · The paper itself

Abstract

Kawasaki disease (KD) is the leading cause of acquired heart disease in children in most developed countries including the United States. The etiology of KD is not known; however, epidemiological and immunological data suggest infectious or immune-related factors in the manifestation of the disease. Further, KD has several hereditary features that strongly suggest a genetic component to disease pathogenesis. Human leucocyte antigen (HLA) loci have also been reported to be associated with KD, but results have been inconsistent, in part, because of small study samples and varying linkage disequilibrium (LD) patterns observed across different ethnic groups. To maximize the informativeness of single nucleotide polymorphism (SNP) genotypes in the major histocompatibility (MHC) region, we imputed classical HLA I (A, B, C) and HLA II (DRB1, DQA1, DQB1) alleles using SNP2HLA method from genotypes of 6700 SNPs within the extended MHC region contained in the ImmunoChip among 112 White patients with KD and their biological parents from North America and tested their association with KD susceptibility using the transmission disequilibrium test. Mendelian consistency in the trios suggested high accuracy and reliability of the imputed alleles (class I = 97.5%, class II = 96.6%). While several SNPs in the MHC region were individually associated with KD susceptibility, we report over-transmission of HLA-C*15 (z = +2.19, P = 0.03) and under-transmission of HLA-B*44 (z = -2.49, P = 0.01) alleles from parents to patients with KD. HLA-B*44 has been associated with KD in other smaller studies, and both HLA-C*15 and HLA-B*44 have biological mechanisms that could potentially be involved in KD pathogenesis. Overall, inferring HLA loci within the same ethnic group, using family-based information is a powerful approach. However, studies with larger sample sizes are warranted to evaluate the correlations of the strength and directions between the SNPs in MHC region and the imputed HLA alleles with KD.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseasePolymorphism, Single NucleotideAllelesFamilyFemaleGene FrequencyHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHumansMaleMucocutaneous Lymph Node SyndromeHistocompatibility Antigens Class IHistocompatibility Antigens Class II

Identifiers

PMID25809546
PMCPMC4430380
OpenAlexW1999483289

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Registered trials

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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.