Evidence map›Paper›PMID 33094923›Full record

ArticleJournal of cellular and molecular medicine2020

Methylprednisolone alleviates multiple sclerosis by expanding myeloid-derived suppressor cells via glucocorticoid receptor β and S100A8/9 up-regulation.

Zhongkun Wang, Ge Zheng, Guangjian Li, Mengkun Wang, Zhanchuan Ma, Huimin Li, Xiang-Yang Wang, Huanfa Yi

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Effects of Psychological Stress on Multiple SclerosisCNS & neurological disorders drug targets · 2024
    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 4 institutions in 2 countries.

Zhongkun WangCentral Laboratory, The First Hospital of Jilin University, Changchun, China.
Ge ZhengHepatopancreatobiliary Surgery Department, The Second Hospital of Jilin University, Changchun, China.
Guangjian LiNeurology Department, The First Hospital of Jilin University, Changchun, China.
Mengkun WangPediatric Department, The First Hospital of Jilin University, Changchun, China.
Zhanchuan MaCentral Laboratory, The First Hospital of Jilin University, Changchun, China.ORCID 0000-0001-8420-6759
Huimin LiCentral Laboratory, The First Hospital of Jilin University, Changchun, China.
Xiang-Yang WangDepartment of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, USA.
Huanfa YiCentral Laboratory, The First Hospital of Jilin University, Changchun, China.
Ministry of Education of the People's Republic of China · CNJilin University · CNSecond Affiliated Hospital of Jilin University · CNVirginia Commonwealth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylprednisolone is an effective drug in the treatment of autoimmune disease, such as multiple sclerosis (MS), due to long-acting anti-inflammatory, antiallergic and immunosuppressant. Previous studies have noted the importance of myeloid-derived suppressor cells (MDSC) in MS progression. However, it is still not known whether methylprednisolone could influence the ratio and function of MDSC during MS treatment. In the current study, we found an increased ratio of MDSC at the onset of EAE in mice model; but methylprednisolone pulse therapy (MPPT) did not alter the percentage and suppressive function of MDSC during disease attenuation. However, the percentage of G-MDSC in PBMC significantly increased in patients with MS. Surprisingly, relapsing MS patients showed a significant increase in both M-MDSC and G-MDSC after MPPT. The disease remission positively correlated expansion of MDSC and expression of arginase-1. Additionally, MPPT reduced the expression of inhibitory glucocorticoid (GCs) receptor β subunit on MDSC while elevating serum levels of immune regulatory S100A8/A9 heterodimer. Thus, MDSC dynamics and function in mouse EAE differ from those in human MS during MPPT. Our study suggested that GCs treatment may help relieve the acute phase of MS by expanding MDSC through up-regulating of GR signalling and S100A8/A9 heterodimers.

Indexed as

AnimalsArginaseBiomarkersCalgranulin ACalgranulin BDisease Models, AnimalDisease SusceptibilityEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryHumansImmunophenotypingLeukocytes, MononuclearMethylprednisoloneMiceMultiple SclerosisMyeloid-Derived Suppressor CellsArg1 protein, mouseArginaseBiomarkersCalgranulin ACalgranulin Bglucocorticoid receptor betaMethylprednisoloneReceptors, Glucocorticoidautoimmune diseasesglucocorticoid receptor βmethylprednisolonemethylprednisolone pulse therapymultiple sclerosismyeloid-derived suppressor cells

Identifiers

PMID33094923
PMCPMC7753844
OpenAlexW3094123792

What OpenQuestion holds

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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.