Evidence map›Paper›PMID 34901814›Full record

ArticleJournal of translational autoimmunity2021

Dissecting the contribution of single nucleotide polymorphisms in

Laura Airaksinen, Juliana Xm Cerqueira, Heini Huhtala, Päivi Saavalainen, Dawit A Yohannes, Markku Mäki, Kalle Kurppa, Elina Kilpeläinen, Anastasia Shcherban, Aarno Palotie and 2 more

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

Article in Journal of translational autoimmunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  4. 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

12 authors at 2 institutions in 3 countries.

Laura AiraksinenCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Juliana Xm CerqueiraCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Heini HuhtalaFaculty of Social Sciences, Tampere University, Tampere, Finland.
Päivi SaavalainenTranslational Immunology Research Program, and Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland.
Dawit A YohannesTranslational Immunology Research Program, and Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland.
Markku MäkiCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Kalle KurppaCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Elina KilpeläinenInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland.
Anastasia ShcherbanInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland.
Aarno PalotieInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland.
Katri KaukinenCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Katri LindforsCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Tampere University · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PURPOSE AND

objectivesGiven their role in homing immune cells to the intestine, CC motif chemokine receptor 9 (CCR9) and its specific ligand CC motif chemokine ligand 25 (CCL25) are interesting candidate genes for celiac disease. These genes are located in regions previously shown to be associated with or linked to celiac disease, but no investigations on their association with various celiac disease phenotypes have so far been conducted. Here we studied such associations of both genotyped and imputed single nucleotide polymorphisms (SNPs) with either regulatory function or exonic location of the

resultsExploiting a carefully phenotyped cohort of 625 celiac disease patients and 1817 non-celiac controls, we identified that multiple SNPs with predicted regulatory function (RegulomeDB score ≤3a and/or eQTL effect) located between 100 kB upstream and downstream of

conclusionsWe conclude that SNPs in the region of

Indexed as

CCL25, CC motif chemokine ligand 25CCR9, CC motif chemokine receptor 9Celiac diseaseChemokine receptorCI, confidence intervalClinical pictureeQTL, expression quantitative trait lociFUMA, Functional Mapping and Annotation of GWASGenetic associationGenetic variationGWAS, genome-wide association studyHLA, human leukocyte antigenHWE, Hardy-Weinberg equilibriumMAF, minor allele frequencyOR, odds ratioPBMC, peripheral blood mononuclear cellQC, quality controlSNP, single nucleotide polymorphismTG2, transglutaminase 2

Identifiers

PMID34901814
PMCPMC8640869
OpenAlexW3205844273

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.