Evidence map›Paper›PMID 37364375›Full record

ArticleMultiple sclerosis and related disorders2023

Targeting miR-223 enhances myeloid-derived suppressor cell suppressive activities in multiple sclerosis patients.

Claudia Cantoni, Laura Ghezzi, Jasmine Choi, Anne H Cross, Laura Piccio

Open access · greenAbstract read
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
1.3field-weighted citation impact, top 19% 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, 8 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Review
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

5 authors at 3 institutions in 3 countries.

Claudia CantoniDepartment of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, United States. Electronic address: claudia.cantoni@barrowneuro.org.
Laura GhezziDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States; Department of Biomedical, Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, 20122 Milan, Italy.
Jasmine ChoiDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Anne H CrossDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Laura PiccioDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, United States; Charles Perkins Centre, School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia.
Washington University in St. Louis · USBarrow Neurological Institute · USUniversity of Milan · IT

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI AIMEE S JAMES · 2001 to 2026
$128.0M
GENETIC MODIFIERS OF CEREBROSPINAL FLUID TREM2 IN ALZHEIMER'S DISEASERF1AG058501 · NIA · WASHINGTON UNIVERSITY · PI CRUCHAGA, CARLOS, PICCIO, LAURA · 2018 to 2018
$3.5M
Genetic Modifiers of TREM2 in Alzheimer's DiseaseR01AG058501 · NIA · WASHINGTON UNIVERSITY · PI Carlos Cruchaga · 2024 to 2026
$2.2M
Intermittent Fasting-induced Gut Microbiome Modulation of CNS AutoimmunityR01NS102633 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ZHOU, YANJIAO · 2017 to 2022
$2.1M
CONSTRUCTION OF EXTRAMURAL RESEARCH FACILITIESC06RR014513 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FISCHBACH, GERALD D · 1999 to 1999
–
NCI NIH HHS P30 CA091842NCRR NIH HHS C06 RR014513NIA NIH HHS R01 AG058501NIA NIH HHS RF1 AG058501NINDS NIH HHS R01 NS102633
6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) is an incurable autoimmune inflammatory demyelinating disease of the central nervous system. Several MS medications can modify disease course through effects on adaptive immune cells, while drugs targeting innate immunity are under investigation. Myeloid-derived suppressor cells (MDSCs) which arise during chronic inflammation, are defined by their T-cell immunosuppressive functions. MiR-223 modulates myeloid cell maturation and expansion, including MDSCs.

methodsMDSCs isolated from healthy controls (HC) and people with MS (pwMS) were co-cultured with CD4+ T-cells to study their immunosuppressive activities in vitro. Cytokines and chemokines concentration were evaluated by Luminex assay in the serum of HC, pwMS, and other neuroinflammatory diseases and correlated with MDSC activities.

resultsMDSC suppressive functions are dysregulated in pwMS compared to HC, which was reversed by glucocorticoids (GC). GC specifically downregulated miR-223 levels in MDSCs and increased the expression of STAT3. In vitro assay showed that miR-223 inhibition enhanced MDSC suppressive activity, STAT3 dependently. By multiple linear regression analysis, we demonstrated that MDSC phosphorylated STAT3 was correlated with serum GM-CSF in HC and pwMS.

conclusionsThese results suggest that miR-223 could be a therapeutic target for enhancing MDSC's suppressive activities as an alternative to GC.

Indexed as

MicroRNAsMultiple SclerosisMyeloid-Derived Suppressor CellsCD4-Positive T-LymphocytesCytokinesHumansImmunosuppressive AgentsCytokinesImmunosuppressive AgentsMicroRNAsMIR223, humanGlucocorticoidsmiR-223Multiple sclerosisMyeloid-derived suppressor cellsNeuroinflammation

Identifiers

PMID37364375
PMCPMC10957070
OpenAlexW4381108625

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.