Evidence map›Paper›PMID 28165503›Full record

ArticleScientific reports2017

Modulation of Microglial Cell Fcγ Receptor Expression Following Viral Brain Infection.

Priyanka Chauhan, Shuxian Hu, Wen S Sheng, Sujata Prasad, James R Lokensgard

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  8. Receptors on Microglia.Advances in neurobiology · 2024
    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

5 authors at 1 institution in 1 country.

Priyanka ChauhanNeurovirology Laboratory, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Shuxian HuNeurovirology Laboratory, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Wen S ShengNeurovirology Laboratory, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Sujata PrasadNeurovirology Laboratory, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
James R LokensgardNeurovirology Laboratory, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
University of Minnesota Medical Center · US

Funding

Role of B-cells and CNS antibodies in modulating chronic microglial activationR01NS038836 · NINDS · UNIVERSITY OF MINNESOTA · PI LOKENSGARD, JAMES R · 2000 to 2022
$7.3M
T lymphocyte-induced glial activation during CNS immune reconstitution diseaseR01MH066703 · NIMH · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LOKENSGARD, JAMES R · 2003 to 2023
$6.9M
NIMH NIH HHS R01 MH066703NINDS NIH HHS R01 NS038836
6 · The paper itself

Abstract

Fcγ receptors (FcγRs) for IgG couple innate and adaptive immunity through activation of effector cells by antigen-antibody complexes. We investigated relative levels of activating and inhibitory FcγRs on brain-resident microglia following murine cytomegalovirus (MCMV) infection. Flow cytometric analysis of microglial cells obtained from infected brain tissue demonstrated that activating FcγRs were expressed maximally at 5 d post-infection (dpi), while the inhibitory receptor (FcγRIIB) remained highly elevated during both acute and chronic phases of infection. The highly induced expression of activating FcγRIV during the acute phase of infection was also noteworthy. Furthermore, in vitro analysis using cultured primary microglia demonstrated the role of interferon (IFN)γ and interleukin (IL)-4 in polarizing these cells towards a M1 or M2 phenotype, respectively. Microglial cell-polarization correlated with maximal expression of either FcγRIV or FcγRIIB following stimulation with IFNγ or IL-4, respectively. Finally, we observed a significant delay in polarization of microglia towards an M2 phenotype in the absence of FcγRs in MCMV-infected Fcer1g and FcgR2b knockout mice. These studies demonstrate that neuro-inflammation following viral infection increases expression of activating FcγRs on M1-polarized microglia. In contrast, expression of the inhibitory FcγRIIB receptor promotes M2-polarization in order to shut-down deleterious immune responses and limit bystander brain damage.

Indexed as

3T3 CellsAnimalsBrainCell DifferentiationCells, CulturedFemaleHerpesviridae InfectionsInterferon-gammaInterleukin-4MiceMice, Inbred BALB CMice, Inbred C57BLMicrogliaMuromegalovirusReceptors, IgGFc gamma receptor IIBInterferon-gammaInterleukin-4Receptors, IgG

Identifiers

PMID28165503
PMCPMC5292951
OpenAlexW2586609554

What Socratic 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 Socratic graph.