Evidence map›Paper›PMID 37806231›Full record

ArticleMultiple sclerosis and related disorders2023

Dysregulation of humoral immunity, iron homeostasis, and lipid metabolism is associated with multiple sclerosis progression.

Qin Wang, Qi Wu, Jennifer Yang, Aiya Saad, Elizabeth Mills, Catherine Dowling, Steven Lundy, Yang Mao-Draayer

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

Article in Multiple sclerosis and related disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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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

8 authors at 1 institution in 1 country.

Qin WangDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Qi WuDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Jennifer YangDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Aiya SaadDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Elizabeth MillsDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Catherine DowlingDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA.
Steven LundyAutoimmunity Center of Excellence, University of Michigan Medical School, USA.
Yang Mao-DraayerDepartment of Neurology, University of Michigan Medical School, USA; Autoimmunity Center of Excellence, University of Michigan Medical School, USA; Graduate Program in Immunology, Program in Biomedical Sciences, University of Michigan Medical School, USA; Michigan Institute for Neurological Disorders, USA. Electronic address: yangmaodraayer@gmail.com.
University of Michigan · US

Funding

University of Michigan Clinical Autoimmunity Center of ExcellenceUM1AI144298 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN, KHANNA, DINESH · 2019 to 2023
$546k
University of Michigan Autoimmunity Center of Excellence, Clinical Research ProgrUM1AI110557 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2014 to 2018
$543k
NIAID NIH HHS UM1 AI110557NIAID NIH HHS UM1 AI144298
6 · The paper itself

Abstract

backgroundThough most patients with multiple sclerosis (MS) presented earlier on as a relapsing-remitting (RR) disease, disability progression eventually occurred. Uncovering the mechanisms underlying progression may facilitate the unmet need for developing therapies to prevent progression. Benign MS (BMS), a rare form of MS, is the opposite from secondary progressive MS (SPMS) in that it lacks disease progression defined as Expanded Disability Status Scale (EDSS) ≤3 after at least 15 years of disease onset. BMS is characterized by rare and mild relapses with complete remission of clinical symptoms (lower activity of the disease) and lack of progression. Our study aims to identify transcriptomic and immunological differences between BMS and SPMS to unravel the pathogenesis of disease progression.

methodsWe took multi-modal approaches with microarrays, flow cytometry, and lipidomics by three-way comparisons of patients with BMS vs. RRMS (low disease activity vs. moderate or severe activity), RRMS vs. SPMS (continued activity vs. complete transformation into progressive phase) as well as BMS vs. SPMS, matched for age and disease-duration (low disease activity and no progression vs. progression with or without activity).

resultsWe found that patients with RRMS and SPMS have a significantly higher percentage of B cells than those with BMS. BMS shows a different transcriptomic profile than SPMS. Many of the differentially expressed genes (DEGs) are involved in B cell-mediated immune responses. Additionally, long-chain fatty acids (LCFA), which can act as inflammatory mediators, are also altered in SPMS. Overall, our data suggest a role for the dysregulation of B cell differentiation and function, humoral immunity, and iron and lipid homeostasis in the pathogenesis of MS disease progression.

conclusionBMS has a unique transcriptomic and immunological profile compared to RRMS and SPMS. These differences will allow for personalized precision medicine and may ultimately lead to the discovery of new therapeutic targets for disease progression.

Indexed as

Multiple SclerosisMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingDisease ProgressionHomeostasisHumansImmunity, HumoralLipid MetabolismBenign multiple sclerosisImmunological signaturesLipidomicsSecondary progressive multiple sclerosisTranscriptomics

Identifiers

PMID37806231
PMCPMC12905824
OpenAlexW4386999117

What OpenQuestion holds

Textmetadata
LicenceTDM
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.