Evidence map›Paper›PMID 26492518›Full record

ArticleGenes and immunity

KIR haplotypes are associated with late-onset type 1 diabetes in European-American families.

J A Traherne, W Jiang, A M Valdes, J A Hollenbach, J Jayaraman, J A Lane, C Johnson, J Trowsdale, J A Noble

Open access · hybridAbstract read
In one paragraph

Article in Genes and immunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. The role of killer-cell immunoglobulin-like receptor (KIR) genes in susceptibility to inflammatory bowel disease: systematic review and meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Pooled it
  3. Review
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  8. MiDAS-Meaningful Immunogenetic Data at Scale.PLoS computational biology · 2021
    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

9 authors at 3 institutions in 2 countries.

J A TraherneDivision of Immunology, Department of Pathology, University of Cambridge, Cambridge, UK.
W JiangCambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
A M ValdesAcademic Rheumatology, University of Nottingham, City Hospital, Nottingham, UK.
J A HollenbachDepartment of Neurology, University of California San Francisco School of Medicine, San Francisco, CA, USA.
J JayaramanCambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
J A LaneChildren's Hospital Oakland Research Institute, Oakland, California, USA.
C JohnsonCambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
J TrowsdaleDivision of Immunology, Department of Pathology, University of Cambridge, Cambridge, UK.
J A NobleChildren's Hospital Oakland Research Institute, Oakland, California, USA.
University of Cambridge · GBUniversity of California, San Francisco · USUniversity of Nottingham · GB

Funding

The genetic basis of type 1 diabetes autoimmunity in African AmericansR01DK061722 · NIDDK · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI NOBLE, JANELLE A · 2003 to 2013
$3.5M
Integrated Exchange & Storage of Current and Future-Generation Immunogenomic DataR01GM109030 · NIGMS · CHILDREN'S HOSPITAL & RES CTR AT OAKLAND · PI HOLLENBACH, JILL ALLISON, MACK, STEVEN JOHN · 2014 to 2016
$919k
Medical Research Council G0901682NIDDK NIH HHS R01 DK061722NIDDK NIH HHS R01 DK61722Wellcome Trust 100140
6 · The paper itself

Abstract

Classical human leukocyte antigens (HLA) genes confer the strongest, but not the only, genetic susceptibility to type 1 diabetes. Killer cell immunoglobulin-like receptors (KIR), on natural killer (NK) cells, bind ligands including class I HLA. We examined presence or absence, with copy number, of KIR loci in 1698 individuals, from 339 multiplex type 1 diabetes families, from the Human Biological Data Interchange, previously genotyped for HLA. Combining family data with KIR copy number information allowed assignment of haplotypes using identity by descent. This is the first disease study to use KIR copy number typing and unambiguously define haplotypes by gene transmission. KIR A1 haplotypes were positively associated with T1D in the subset of patients without the high T1D risk HLA genotype, DR3/DR4 (odds ratio=1.29, P=0.0096). The data point to a role for KIR in type 1 diabetes risk in late-onset patients. In the top quartile (age of onset>14), KIR A2 haplotype was overtransmitted (63.4%, odds ratio=1.73, P=0.024) and KIR B haplotypes were undertransmitted (41.1%, odds ratio=0.70, P=0.0052) to patients. The data suggest that inhibitory 'A' haplotypes are predisposing and stimulatory 'B' haplotypes confer protection in both DR3/DR4-negative and late-onset patient groups.

Indexed as

Genetic Predisposition to DiseaseAge of OnsetChildDiabetes Mellitus, Type 1FemaleGenetic Association StudiesHaplotypesHLA AntigensHumansMaleReceptors, KIRWhite PeopleHLA AntigensReceptors, KIR

Identifiers

PMID26492518
PMCPMC4746488
OpenAlexW2175178469

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.