Evidence map›Paper›PMID 17513529›Full record

ArticleJournal of medical genetics2007

A functional CD86 polymorphism associated with asthma and related allergic disorders.

Thomas Juhl Corydon, Annette Haagerup, Thomas Gryesten Jensen, Helle Glud Binderup, Mikkel Steen Petersen, Keld Kaltoft, Jørgen Vestbo, Torben Arvid Kruse, Anders Dupont Børglum

Open access · greenAbstract read
In one paragraph

Article in Journal of medical genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Molecular therapy. Nucleic acids · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. CD86 gene variants and susceptibility to pancreatic cancer.Journal of cancer research and clinical oncology · 2012
    Article
  10. Review
  11. Article
  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

9 authors at 3 institutions in 2 countries.

Thomas Juhl CorydonInstitute of Human Genetics, the Bartholin Building, University of Aarhus, DK-8000 Aarhus C, Denmark.
Annette Haagerup
Thomas Gryesten Jensen
Helle Glud Binderup
Mikkel Steen Petersen
Keld Kaltoft
Jørgen Vestbo
Torben Arvid Kruse
Anders Dupont Børglum
Aarhus University · DKUniversity of Southern Denmark · DKWythenshawe Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral studies have documented a substantial genetic component in the aetiology of allergic diseases and a number of atopy susceptibility loci have been suggested. One of these loci is 3q21, at which linkage to multiple atopy phenotypes has been reported. This region harbours the CD86 gene encoding the costimulatory B7.2 protein. The costimulatory system, consisting of receptor proteins, cytokines and associated factors, activates T cells and regulates the immune response upon allergen challenge.

methodsWe sequenced the CD86 gene in patients with atopy from 10 families that showed evidence of linkage to 3q21. Identified polymorphisms were analysed in a subsequent family-based association study of two independent Danish samples, respectively comprising 135 and 100 trios of children with atopy and their parents. Functional analysis of the costimulatory effect on cytokine production was performed in an autologous cell-based system based on cells expressing CD86 variants.

resultsTwo polymorphisms were identified, encoding the amino acid changes Ile179Val and Ala304Thr, respectively. Significant associations were observed between the Ile179Val polymorphism and allergy phenotypes in both samples (eg, asthma, p = 4 x 10(-3) in the two samples combined). The undertransmitted (protective) Val179 allele was found to induce higher production of both Th1 and Th2 cytokines than the overtransmitted (risk) Ile179 allele, suggesting a functional impact of the polymorphism.

conclusionThe CD86 gene, and specifically the Ile179Val polymorphism, may be a novel aetiological factor in the development of asthma and related allergic disorders.

Indexed as

Chromosomes, Human, Pair 3Amino Acid SubstitutionAntigens, CDAsthmaB7-2 AntigenCell LineCell Line, TumorCloning, MolecularFemaleGenetic LinkageGenetic VariationHumansHypersensitivityMaleMelanomaPolymorphism, GeneticAntigens, CDB7-2 Antigen

Identifiers

PMID17513529
PMCPMC2597931
OpenAlexW2126703363

What OpenQuestion holds

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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.