Evidence map›Paper›PMID 18781189›Full record

SynthesisEuropean journal of human genetics : EJHG2009

Meta-analysis of genome-wide linkage studies across autoimmune diseases.

Paola Forabosco, Emmanuelle Bouzigon, Mandy Y Ng, Jane Hermanowski, Sheila A Fisher, Lindsey A Criswell, Cathryn M Lewis

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in European journal of human genetics : EJHG, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Polymorphisms in theCanine medicine and genetics · 2020
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The multiple autoimmune syndromes. A clue for the autoimmune tautology.Clinical reviews in allergy & immunology · 2012
    Article
  13. Article
  14. The immunogenetic architecture of autoimmune disease.Cold Spring Harbor perspectives in biology · 2012
    Review
  15. Article
  16. 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

7 authors at 3 institutions in 3 countries.

Paola ForaboscoKing's College London School of Medicine, Department of Medical and Molecular Genetics, London, UK.
Emmanuelle Bouzigon
Mandy Y Ng
Jane Hermanowski
Sheila A Fisher
Lindsey A Criswell
Cathryn M Lewis
King's College London · GBInserm · FRUniversity of California, San Francisco · US

Funding

MAPPING OF NON-HLA LOCI FOR GLUTEN SENSITIVE ENTEROPATHYR01DK050678 · NIDDK · UNIVERSITY OF UTAH · PI NEUHAUSEN, SUSAN L. · 1996 to 2005
$2.7M
The Genetic Epidemiology of RA and SLEK24AR002175 · NIAMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CRISWELL, LINDSEY ANN · 2001 to 2005
$555k
Medical Research Council G0400960NIAMS NIH HHS K24 AR002175NIAMS NIH HHS K24 AR02175NIDDK NIH HHS DK50678NIDDK NIH HHS R01 DK050678
6 · The paper itself

Abstract

Autoimmune diseases are chronic disorders initiated by a loss of immunologic tolerance to self-antigens. They cluster within families, and patients may be diagnosed with more than one disease, suggesting pleiotropic genes are involved in the aetiology of different diseases. To identify potential loci, which confer susceptibility to autoimmunity independent of disease phenotype, we pooled results from genome-wide linkage studies, using the genome scan meta-analysis method (GSMA). The meta-analysis included 42 independent studies for 11 autoimmune diseases, using 7350 families with 18 291 affected individuals. In addition to the HLA region, which showed highly significant genome-wide evidence for linkage, we obtained suggestive evidence for linkage on chromosome 16, with peak evidence at 10.0-19.8 Mb. This region may harbour a pleiotropic gene (or genes) conferring risk for several diseases, although no such gene has been identified through association studies. We did not identify evidence for linkage at several genes known to confer increased risk to different autoimmune diseases (PTPN22, CTLA4), even in subgroups of diseases consistently found to be associated with these genes. The relative risks conferred by variants in these genes are modest (<1.5 in most cases), and even a large study like this meta-analysis lacks power to detect linkage. This study illustrates the concept that linkage and association studies have power to identify very different types of disease-predisposing variants.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyAutoimmune DiseasesHumansMajor Histocompatibility Complex

Identifiers

PMID18781189
PMCPMC2986058
OpenAlexW2074654175

What OpenQuestion holds

Textmetadata
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.