Evidence map›Paper›PMID 32793234›Full record

ArticleFrontiers in immunology2020

M1 Macrophage Derived Exosomes Aggravate Experimental Autoimmune Neuritis via Modulating Th1 Response.

Tong Du, Chun-Lin Yang, Meng-Ru Ge, Ying Liu, Peng Zhang, Heng Li, Xiao-Li Li, Tao Li, Yu-Dong Liu, Ying-Chun Dou and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Review
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  3. Salidroside ameliorates experimental autoimmune neuritis by dually modulating neuroinflammation and immune homeostasis via PI3K/AKT signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

12 authors.

Tong DuDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Chun-Lin YangDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Meng-Ru GeDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Ying LiuDepartment of Neuronal Electrophysiology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Peng ZhangDepartment of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Heng LiDepartment of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Xiao-Li LiDepartment of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Tao LiDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Yu-Dong LiuDepartment of Neuronal Electrophysiology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Ying-Chun DouCollege of Basic Medical Sciences, Shandong University of Traditional Chinese Medicine, Jinan, China.
Bing YangDepartment of Neurology, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Rui-Sheng DuanDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Guillain-Barré syndrome (GBS), an immune-mediated disorder affecting the peripheral nervous system, is the most common and severe acute paralytic neuropathy. GBS remains to be potentially life-threatening and disabling despite the increasing availability of current standard therapeutic regimens. Therefore, more targeted therapeutics are in urgent need. Macrophages have been implicated in both initiation and resolution of experimental autoimmune neuritis (EAN), the animal model of GBS, but the exact mechanisms remain to be elucidated. It has been increasingly appreciated that exosomes, a type of extracellular vesicles (EVs), are of importance for functions of macrophages. Nevertheless, the roles of macrophage derived exosomes in EAN/GBS remain unclear. Here we determined the effects of macrophage derived exosomes on the development of EAN in Lewis rats. M1 macrophage derived exosomes (M1 exosomes) were found to aggravate EAN via boosting Th1 and Th17 response, while M2 macrophage derived exosomes (M2 exosomes) showed potentials to mitigate disease severity via a mechanism bypassing Th1 and Th17 response. Besides, both M1 and M2 exosomes increased germinal center reactions in EAN. Further

Indexed as

AnimalsDisease ProgressionExosomesFemaleGerminal CenterGuillain-Barre SyndromeImmunity, CellularImmunity, InnateInterferon-gammaMacrophage ActivationMacrophagesNeuritis, Autoimmune, ExperimentalRats, Inbred LewTh17 CellsTh1 CellsT-LymphocytesInterferon-gammaexosomesexperimental autoimmune neuritis (EAN)Guillain–Barré syndrome (GBS)IFN-γmacrophagesT helper 1 (Th1) cells

Identifiers

PMID32793234
PMCPMC7390899

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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.