Evidence map›Paper›PMID 29904389›Full record

ArticleFrontiers in immunology2018

RhoA Drives T-Cell Activation and Encephalitogenic Potential in an Animal Model of Multiple Sclerosis.

Alba Manresa-Arraut, Flemming Fryd Johansen, Cord Brakebusch, Shohreh Issazadeh-Navikas, Henrik Hasseldam

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. 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
2.1field-weighted citation impact, top 13% 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, 32 citations in OpenAlex.

  1. Nasal administration of anti-CD3 mAb (Foralumab) downregulatesProceedings of the National Academy of Sciences of the United States of America · 2023
    Trial
  2. Article
  3. Article
  4. Review
  5. RhoG's Role in T Cell Activation and Function.Frontiers in immunology · 2022
    Review
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. HaploinsufficientCells · 2020
    Article
  14. Review
  15. Article
  16. Article
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.

Alba Manresa-ArrautNeuroinflammation Unit, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Flemming Fryd JohansenNeuroinflammation Unit, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Cord BrakebuschCytoskeletal Organization Group, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Shohreh Issazadeh-NavikasNeuroinflammation Unit, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Henrik HasseldamNeuroinflammation Unit, Biotech Research and Innovation Centre (BRIC), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cells are known to be intimately involved in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). T-cell activation is controlled by a range of intracellular signaling pathways regulating cellular responses such as proliferation, cytokine production, integrin expression, and migration. These processes are crucial for the T-cells' ability to mediate inflammatory processes in autoimmune diseases such as MS. RhoA is a ubiquitously expressed small GTPase well described as a regulator of the actin cytoskeleton. It is essential for embryonic development and together with other Rho GTPases controls various cellular processes such as cell development, shaping, proliferation, and locomotion. However, the specific contribution of RhoA to these processes in T-cells in general, and in autoreactive T-cells in particular, has not been fully characterized. Using mice with a T-cell specific deletion of the RhoA gene (RhoA

Indexed as

Disease SusceptibilityAnimalsAntigensBiomarkersCytokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalImmunohistochemistryImmunophenotypingLymphocyte ActivationMiceMice, KnockoutMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinrhoA GTP-Binding ProteinT-LymphocytesAntigensBiomarkersCytokinesMyelin-Oligodendrocyte GlycoproteinrhoA GTP-Binding Proteinexperimental autoimmune encephalomyelitismultiple sclerosisneuroinflammationRhoAT-cell

Identifiers

PMID29904389
PMCPMC5990621
OpenAlexW2804679393

What OpenQuestion holds

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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.