Evidence map›Paper›PMID 21179112›Full record

ArticleGenes and immunity2011

Exploring the CLEC16A gene reveals a MS-associated variant with correlation to the relative expression of CLEC16A isoforms in thymus.

I-L Mero, M Ban, Å R Lorentzen, C Smestad, E G Celius, H Sæther, H Saeedi, M K Viken, B Skinningsrud, D E Undlien and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025
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  5. International journal of molecular sciences · 2023
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  9. Review
  10. Frontiers in genetics · 2022
    Article
  11. Article
  12. Article
  13. The Autoimmune Disorder Susceptibility GeneFrontiers in immunology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. 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

18 authors at 4 institutions in 2 countries.

I-L MeroDepartment of Neurology, Oslo University Hospital, Oslo, Norway. ilmero@rr-research.no
M Ban
Å R Lorentzen
C Smestad
E G Celius
H Sæther
H Saeedi
M K Viken
B Skinningsrud
D E Undlien
J Aarseth
K-M Myhr
S Granum
A Spurkland
S Sawcer
A Compston
B A Lie
H F Harbo
Oslo University Hospital · NOUniversity of Oslo · NOUniversity of Cambridge · GBHaukeland University Hospital · NO

Funding

Medical Research Council G0000934Medical Research Council G0700061Wellcome Trust 068545/Z/02.Wellcome Trust 076113Wellcome Trust 084702Wellcome Trust 084702/Z/08/Z
6 · The paper itself

Abstract

Genomewide association studies have implicated the CLEC16A gene in several autoimmune diseases, including multiple sclerosis (MS) and type 1 diabetes. However, the most associated single-nucleotide polymorphism (SNP) varies, and causal variants are still to be defined. In MS, two SNPs in partial linkage disequilibrium with each other, rs6498169 and rs12708716, have been validated at genomewide significance level. To explore the CLEC16A association in MS in more detail, we genotyped 57 SNPs in 807 Norwegian MS patients and 1027 Norwegian controls. Six highly associated SNPs emerged and were then replicated in two large independent sample sets (Norwegian and British), together including 1153 MS trios, 2308 MS patients and 4044 healthy controls. In combined analyses, SNP rs12708716 gave the strongest association signal in MS (P=5.3 x 10⁻⁸, odds ratio 1.18, 95% confidence interval=1.11-1.25), and was found to be superior to the other SNP associations in conditional logistic regression analyses. Expression analysis revealed that rs12708716 genotype was significantly associated with the relative expression levels of two different CLEC16A transcripts in thymus (P=0.004), but not in blood, possibly implying a thymus- or cell-specific splice regulation.

Indexed as

Gene Expression RegulationAdultAllelesFemaleGene Expression ProfilingGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansLectins, C-TypeMaleMiddle AgedMonosaccharide Transport ProteinsMultiple SclerosisPolymorphism, Single NucleotideCLEC16A protein, humanLectins, C-TypeMonosaccharide Transport ProteinsProtein Isoforms

Identifiers

PMID21179112
OpenAlexW2050418148

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.