Evidence map›Paper›PMID 33426702›Full record

ArticleClinical and experimental immunology2021

Adoptive transfer of immunomodulatory M2 macrophages suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice via blockading NF-κB pathway.

F Chu, M Shi, Y Lang, Z Chao, T Jin, L Cui, J Zhu

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  13. The neurotropic schistosomeParasitology · 2024
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  15. A new era of macrophage-based cell therapy.Experimental & molecular medicine · 2023
    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

7 authors at 2 institutions in 2 countries.

F Chu *Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.ORCID 0000-0003-3291-1768
M Shi *Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.
Y LangDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.
Z ChaoDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.
T JinDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.ORCID 0000-0002-7028-3419
L CuiDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.
J ZhuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin Province, China.
Jilin University · CNKarolinska University Hospital · SE

Funding

International Science and Technology Cooperation Program of Jilin Provincial Science and Technology Development of China 20150414011GHNational Natural Science Foundation of China 31600820National Natural Science Foundation of China 81471216National Natural Science Foundation of China 81671177National Natural Science Foundation of China 81671186Norman Bethune Cultivation Plan of Jilin University 2015320
6 · The paper itself

Abstract

Macrophages play important roles in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), and M2 macrophage may have anti-inflammatory effects. In this study, we elucidated the roles of M1 and M2 macrophages in the pathogenesis of EAE and the effects of treatment with M2 macrophages that target certain proinflammatory cytokines and with immunomodulatory preparations that beneficially influence the disease course. We found macrophages increased at the onset of clinical signs in the EAE group, consistent with an increased proportion of M1 macrophages and low numbers of M2 macrophages. As the disease progressed and the symptoms worsened, M1 macrophages decreased and M2 macrophages gradually increased until the peak. In the recovery stage, M2 macrophages gradually decreased. Treatment with M2 macrophages inhibited the nuclear factor kappa B (NF-κB) pathway, alleviated the symptoms of EAE, reduced inflammatory cell infiltration and demyelination in the central nervous system and decreased the numbers of macrophages in the spleens. BAY-11-7082, an NF-κB blocking agent, could reduce the total number of macrophages both in vivo and in vitro, effectively prevented EAE development and significantly inhibited EAE symptoms in mice. Our study demonstrates that macrophages may play a crucial role in the pathogenesis of EAE, while M2 macrophages have anti-inflammatory effects. Transfer of M2 macrophages to EAE mice can block the NF-κB pathway successfully and relieve EAE symptoms. Application of NF-κB blockers is useful in the prevention and treatment of EAE.

Indexed as

Adoptive TransferAnimalsCentral Nervous SystemCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunomodulationInflammationMacrophagesMiceMice, Inbred C57BLMultiple SclerosisNF-kappa BSignal TransductionCytokinesNF-kappa Bcell transferEAEM2 macrophagesNF-κBtherapy

Identifiers

PMID33426702
PMCPMC8062990
OpenAlexW3120085086

What OpenQuestion holds

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Registered trials

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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.