Evidence map›Paper›PMID 22586495›Full record

ArticlePloS one2012

Importance of human leukocyte antigen (HLA) class I and II alleles on the risk of multiple sclerosis.

Jenny Link, Ingrid Kockum, Aslaug R Lorentzen, Benedicte A Lie, Elisabeth G Celius, Helga Westerlind, Marie Schaffer, Lars Alfredsson, Tomas Olsson, Boel Brynedal and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Endogenous Retroviruses in Nervous System Disorders.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Extracellular vesicle fibrinogen induces encephalitogenic CD8+ T cells in a mouse model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
  14. Genetic risk factors for pediatric-onset multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Sex and gender issues in multiple sclerosis.Therapeutic advances in neurological disorders · 2013
    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

12 authors at 3 institutions in 2 countries.

Jenny LinkDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. jenny.link@ki.se
Ingrid Kockum
Aslaug R Lorentzen
Benedicte A Lie
Elisabeth G Celius
Helga Westerlind
Marie Schaffer
Lars Alfredsson
Tomas Olsson
Boel Brynedal
Hanne F Harbo
Jan Hillert
Karolinska Institutet · SEOslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a complex disease of the central nervous system of unknown etiology. The human leukocyte antigen (HLA) locus on chromosome 6 confers a considerable part of the susceptibility to MS, and the most important factor is the class II allele HLA-DRB1*15:01. In addition, we and others have previously established a protective effect of HLA-A*02. Here, we genotyped 1,784 patients and 1,660 healthy controls from Scandinavia for the HLA-A, HLA-B, HLA-C and HLA-DRB1 genes and investigated their effects on MS risk by logistic regression. Several allele groups were found to exert effects independently of DRB1*15 and A*02, in particular DRB1*01 (OR = 0.82, p = 0.034) and B*12 (including B*44/45, OR = 0.76, p = 0.0028), confirming previous reports. Furthermore, we observed interaction between allele groups: DRB1*15 and DRB1*01 (multiplicative: OR = 0.54, p = 0.0041; additive: AP = 0.47, p = 4 × 10(-06)), DRB1*15 and C*12 (multiplicative: OR = 0.37, p = 0.00035; additive: AP = 0.58, p = 2.6 × 10(-05)), indicating that the effect size of these allele groups varies when taking DRB1*15 into account. Analysis of inferred haplotypes showed that almost all DRB1*15 bearing haplotypes were risk haplotypes, and that all A*02 bearing haplotypes were protective as long as they did not carry DRB1*15. In contrast, we found one class I haplotype, carrying A*02-C*05-B*12, which abolished the risk of DRB1*15. In conclusion, these results confirms a complex role of HLA class I and II genes that goes beyond DRB1*15 and A*02, in particular by including all three classical HLA class I genes as well as functional interactions between DRB1*15 and several alleles of DRB1 and class I genes.

Indexed as

HLA-A AntigensHLA-B AntigensAdultAgedAged, 80 and overAllelesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHaplotypesHLA-DRB1 ChainsHumansLinkage DisequilibriumMaleMiddle AgedMultiple SclerosisHLA-A AntigensHLA-B AntigensHLA-DRB1 Chains

Identifiers

PMID22586495
PMCPMC3346735
OpenAlexW2032345322

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.