Is DEXI a Multiple Sclerosis Susceptibility Gene?

Anna M Eriksson, Nora Emini, Hanne F Harbo, Tone Berge

Abstract readReview

In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it

0cells of the map it votes in

2citing 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

2 citing papers in PubMed.

Mechanism of action and clinical application of autophagy in multiple sclerosis (Review).International journal of molecular medicine · 2026
Review
Genome-scale mapping of variant, enhancer and gene function in primary human CD4+ T cells.bioRxiv : the preprint server for biology · 2026
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.

Anna M ErikssonInstitute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0450 Oslo, Norway.

Nora EminiDepartment of Research, Innovation and Education, Oslo University Hospital, Kirkeveien 166, 0450 Oslo, Norway.

Hanne F HarboInstitute of Clinical Medicine, University of Oslo, Kirkeveien 166, 0450 Oslo, Norway.ORCID 0000-0002-6047-0122

Tone BergeDepartment of Research, Innovation and Education, Oslo University Hospital, Kirkeveien 166, 0450 Oslo, Norway.

Funding

University of Oslo xxx

6 · The paper itself

Abstract

The genetic landscape of multiple sclerosis (MS) has been extensively mapped, yielding significant insights into the molecular mechanisms of the disorder. Early studies highlighted key genes associated with the immune system, particularly T cells, as critical for MS susceptibility. Subsequent large-scale genome-wide association studies (GWASs) identified over 200 genetic variants linked to MS, revealing a complex interplay between MS risk and genes involved in various processes within adaptive and innate immune cells, as well as brain-resident microglia. Recently, a groundbreaking GWAS pinpointed the first gene variant associated with MS disease progression, distinguishing the mechanisms driving disease onset from those influencing progression. The C-type lectin domain family 16, member A (

Indexed as

Genetic Predisposition to DiseaseLectins, C-TypeMonosaccharide Transport ProteinsMultiple SclerosisAnimalsGenome-Wide Association StudyHumansQuantitative Trait LociCLEC16A protein, humanLectins, C-TypeMonosaccharide Transport ProteinsautoimmunityCLEC16ADEXImultiple sclerosissusceptibility genes

Identifiers

PMID39940946

DOI10.3390/ijms26031175

PMCPMC11818924

What OpenQuestion holds

Textmetadata

LicenceCC BY

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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.