Evidence map›Paper›PMID 34246256›Full record

ArticleBMC medical genomics2021

Genetic susceptibility to multiple sclerosis: interactions between conserved extended haplotypes of the MHC and other susceptibility regions.

D S Goodin, P Khankhanian, P A Gourraud, N Vince

Abstract read
In one paragraph

Article in BMC medical genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Pathogenesis of multiple sclerosis: genetic, environmental and random mechanisms.Journal of neurology, neurosurgery, and psychiatry · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

4 authors.

D S GoodinDepartment of Neurology, University of California, UCSF MS Center, San Francisco 675 Nelson Rising Lane, Suite #221D, CA, 94158, San Francisco, USA. douglas.goodin@ucsf.edu.ORCID 0000-0002-5985-0822
P KhankhanianCenter for Neuro-Engineering and Therapeutics, University of Pennsylvania, Philadelphia, PA, USA.
P A GourraudDepartment of Neurology, University of California, UCSF MS Center, San Francisco 675 Nelson Rising Lane, Suite #221D, CA, 94158, San Francisco, USA.
N VinceCentre de Recherche en Transplantation Et Immunologie, UMR 1064, INSERM, Université de Nantes, Nantes, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo study the accumulation of MS-risk resulting from different combinations of MS-associated conserved-extended-haplotypes (CEHs) of the MHC and three non-MHC "risk-haplotypes" nearby genes EOMES, ZFP36L1, and CLEC16A. Many haplotypes are MS-associated despite having population-frequencies exceeding the percentage of genetically-susceptible individuals. The basis of this frequency-disparity requires explanation.

methodsThe SNP-data from the WTCCC was phased at the MHC and three non-MHC susceptibility-regions. CEHs at the MHC were classified into five haplotype-groups: (HLA-DRB1*15:01 ~ DQB1*06:02 ~ a1)-containing (H +); extended-risk (ER); all-protective (AP); neutral (0); and the single-CEH (c1). MS-associations for different "risk-combinations" at the MHC and other non-MHC "risk-loci" and the appropriateness of additive and multiplicative risk-accumulation models were assessed.

resultsDifferent combinations of "risk-haplotypes" produce a final MS-risk closer to additive rather than multiplicative risk-models but neither model was consistent. Thus, (H +)-haplotypes had greater impact when combined with (0)-haplotypes than with (H +)-haplotypes, whereas, (H +)-haplotypes had greater impact when combined with a (c1)-haplotypes than with (0)-haplotypes. Similarly, risk-genotypes (0,H +), (c1,H +), (H + ,H +) and (0,c1) were additive with risks from non-MHC risk-loci, whereas risk-genotypes (ER,H +) and (AP,c1) were unaffected.

conclusionsGenetic-susceptibility to MS is essential for MS to develop but actually developing MS depends heavily upon both an individual's particular combination of "risk-haplotypes" and how these loci interact.

Indexed as

Genetic Predisposition to DiseaseHaplotypesMultiple SclerosisPolymorphism, Single NucleotideHumansMajor Histocompatibility ComplexAdditiveCombinationEpidemiologyGeneticMultiple sclerosisMultiplicativeRiskSusceptibility

Identifiers

PMID34246256
PMCPMC8272333

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.