Evidence map›Paper›PMID 29485127›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Norepinephrine Inhibits Th17 Cells via β2-Adrenergic Receptor (β2-AR) Signaling in a Mouse Model of Rheumatoid Arthritis.

Yan Liu, Xiao-Xiao Rui, Hui Shi, Yi-Hua Qiu, Yu-Ping Peng

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-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

24 citing papers in PubMed, 28 citations in OpenAlex.

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  15. The Dual Role of the βInternational journal of molecular sciences · 2022
    Article
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  18. Driving βFrontiers in immunology · 2021
    Article
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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

5 authors at 2 institutions in 1 country.

Yan LiuSchool of Biological and Basic Medical Sciences, Soochow University, Suzhou, Jiangsu, China (mainland).
Xiao-Xiao RuiDepartment of Physiology, School of Medicine, and Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China (mainland).
Hui ShiDepartment of Physiology, School of Medicine, and Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China (mainland).
Yi-Hua QiuDepartment of Physiology, School of Medicine, and Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China (mainland).
Yu-Ping PengDepartment of Physiology, School of Medicine, and Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China (mainland).
Nantong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Norepinephrine (NE), a neurotransmitter released from the sympathetic nerves, has been shown to be involved in rheumatoid arthritis (RA). However, its role in the sympathetic nervous system in RA is divergent. Herein, we demonstrate that the sympathetic neurotransmitter NE exerts an anti-inflammatory effect in collagen-induced arthritis (CIA), a mouse model of RA, by inhibiting Th17 cell differentiation and function via β2-adrenergic receptor (β2-AR) signaling. MATERIAL AND METHODS CIA was prepared by intradermal injection of collagen type II in the tail base of DBA1/J mice. On the 41st day post-immunization, the mice were used as CIA models. CD4+ T cells from the spleen were purified using magnetic cell sorting and activated with anti-CD3 anti-CD28 antibodies. Th17 cells were polarized from the CD4+ T cells using various antibodies and cytokines. RESULTS Co-expression of CD4 and β2-AR was observed in spleens of both intact and CIA mice. The β2-AR expression in the ankle and spleen was downregulated in CIA mice. CIA induced increases in production of interleukin (IL)-17 and IL-22, CD25-IL-17+ cell percentage, and ROR-γt expression in CD4+ T cells. Importantly, NE reduced the CIA-induced CD4+ T cell shift towards Th17 phenotype, and the β2-AR antagonist ICI118551 blocked the NE effect. Moreover, the β2-AR agonist terbutaline (Terb) inhibited CIA-induced CD4+ T cell proliferation and shift towards Th17 phenotype, and the protein kinase A (PKA) inhibitor H-89 abolished the agonist effect. Terb also reduced CIA-induced Th17 enhancement, and H-89 impaired the Terb effect. CONCLUSIONS NE inhibits Th17 cell differentiation and function in CIA condition by activation of β2-AR/PKA signaling.

Indexed as

Adrenergic beta-2 Receptor AgonistsAnimalsArthritis, RheumatoidCyclic AMP-Dependent Protein KinasesDisease Models, AnimalDown-RegulationMaleMiceNorepinephrinePhenotypeProtein Kinase InhibitorsReceptors, Adrenergic, beta-2Signal TransductionTh17 CellsAdrenergic beta-2 Receptor AgonistsCyclic AMP-Dependent Protein KinasesNorepinephrineProtein Kinase InhibitorsReceptors, Adrenergic, beta-2

Identifiers

PMID29485127
PMCPMC5839072
OpenAlexW2788378244

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.