Evidence map›Paper›PMID 29081780›Full record

ArticleFrontiers in immunology2017

Deletion of the Mineralocorticoid Receptor in Myeloid Cells Attenuates Central Nervous System Autoimmunity.

Elena Montes-Cobos, Nils Schweingruber, Xiao Li, Henrike J Fischer, Holger M Reichardt, Fred Lühder

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Elena Montes-CobosInstitute for Cellular and Molecular Immunology, University Medical Center Goettingen, Goettingen, Germany.
Nils SchweingruberInstitute for Cellular and Molecular Immunology, University Medical Center Goettingen, Goettingen, Germany.
Xiao LiInstitute for Cellular and Molecular Immunology, University Medical Center Goettingen, Goettingen, Germany.
Henrike J FischerInstitute for Cellular and Molecular Immunology, University Medical Center Goettingen, Goettingen, Germany.
Holger M ReichardtInstitute for Cellular and Molecular Immunology, University Medical Center Goettingen, Goettingen, Germany.
Fred LühderInstitute of Neuroimmunology, University Medical Center Goettingen, Goettingen, Germany.
University of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid cells play an important role in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Monocytes, macrophages, and microglia can adopt two distinct phenotypes, with M1-polarized cells being more related to inflammation and autoimmunity while M2-polarized cells contribute to tissue repair and anti-inflammatory processes. Here, we show that deletion of the mineralocorticoid receptor (MR) in bone marrow-derived macrophages and peritoneal macrophages caused their polarization toward the M2 phenotype with its distinct gene expression, altered phagocytic and migratory properties, and dampened NO production. After induction of EAE, mice that are selectively devoid of the MR in their myeloid cells (MR

Indexed as

experimental autoimmune encephalomyelitisM2 polarizationmineralocorticoid receptormyeloid cellsneuroinflammation

Identifiers

PMID29081780
PMCPMC5645513
OpenAlexW2762029453

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.