Evidence map›Paper›PMID 26941483›Full record

ReviewMediators of inflammation2016

Th17 Cells Pathways in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders: Pathophysiological and Therapeutic Implications.

Giordani Rodrigues Dos Passos, Douglas Kazutoshi Sato, Jefferson Becker, Kazuo Fujihara

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 148 citations in OpenAlex.

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  18. CD4Cells · 2024
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23 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Giordani Rodrigues Dos PassosBrain Institute and Department of Neurology, Faculty of Medicine, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Avenida Ipiranga 6690, 90610-000 Porto Alegre, RS, Brazil.
Douglas Kazutoshi SatoBrain Institute and Department of Neurology, Faculty of Medicine, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Avenida Ipiranga 6690, 90610-000 Porto Alegre, RS, Brazil; Department of Neurology and LIM-15, Faculty of Medicine, University of Sao Paulo (USP), Avenida Dr. Arnaldo 455, 01246-903 São Paulo, SP, Brazil; Department of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai, Miyagi 980-8574, Japan.
Jefferson BeckerBrain Institute and Department of Neurology, Faculty of Medicine, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Avenida Ipiranga 6690, 90610-000 Porto Alegre, RS, Brazil.
Kazuo FujiharaDepartment of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai, Miyagi 980-8574, Japan.
Pontifícia Universidade Católica do Rio Grande do Sul · BRTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several animal and human studies have implicated CD4+ T helper 17 (Th17) cells and their downstream pathways in the pathogenesis of central nervous system (CNS) autoimmunity in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD), challenging the traditional Th1-Th2 paradigm. Th17 cells can efficiently cross the blood-brain barrier using alternate ways from Th1 cells, promote its disruption, and induce the activation of other inflammatory cells in the CNS. A number of environmental factors modulate the activity of Th17 pathways, so changes in the diet, exposure to infections, and other environmental factors can potentially change the risk of development of autoimmunity. Currently, new drugs targeting specific points of the Th17 pathways are already being tested in clinical trials and provide basis for the development of biomarkers to monitor disease activity. Herein, we review the key findings supporting the relevance of the Th17 pathways in the pathogenesis of MS and NMOSD, as well as their potential role as therapeutic targets in the treatment of immune-mediated CNS disorders.

Indexed as

AnimalsCentral Nervous SystemHumansMultiple SclerosisNeuromyelitis OpticaTh17 Cells

Identifiers

PMID26941483
PMCPMC4749822
OpenAlexW2277589202

What OpenQuestion holds

Textmetadata
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.