Evidence map›Paper›PMID 32240164›Full record

ArticlePloS one2020

Genetic deletion of Autotaxin from CD11b+ cells decreases the severity of experimental autoimmune encephalomyelitis.

Ioanna Ninou, Ioanna Sevastou, Christiana Magkrioti, Eleanna Kaffe, George Stamatakis, Spyros Thivaios, George Panayotou, Junken Aoki, George Kollias, Vassilis Aidinis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Autotaxin Has a Negative Role in Systemic Inflammation.International journal of molecular sciences · 2022
    Article
  12. Design and Development of Autotaxin Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  13. Article
  14. Review
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

10 authors at 2 institutions in 2 countries.

Ioanna NinouBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Ioanna SevastouBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Christiana MagkriotiBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Eleanna KaffeBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
George StamatakisBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Spyros ThivaiosBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
George PanayotouBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Junken AokiGraduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
George KolliasBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Vassilis AidinisBiomedical Sciences Research Center Alexander Fleming, Athens, Greece.ORCID 0000-0001-9531-7729
Alexander Fleming Biomedical Sciences Research Center · GRTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autotaxin (ATX) is a secreted lysophospholipase D catalyzing the extracellular production of lysophosphatidic acid (LPA), a growth factor-like signaling lysophospholipid. ATX and LPA signaling have been incriminated in the pathogenesis of different chronic inflammatory diseases and various types of cancer. In this report, deregulated ATX and LPA levels were detected in the spinal cord and plasma of mice during the development of experimental autoimmune encephalomyelitis (EAE). Among the different sources of ATX expression in the inflamed spinal cord, F4/80+ CD11b+ cells, mostly activated macrophages and microglia, were found to express ATX, further suggesting an autocrine role for ATX/LPA in their activation, an EAE hallmark. Accordingly, ATX genetic deletion from CD11b+ cells attenuated the severity of EAE, thus proposing a pathogenic role for the ATX/LPA axis in neuroinflammatory disorders.

Indexed as

AnimalsCD11b AntigenCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalGene DeletionGene ExpressionHumansLysophospholipase DLysophospholipidsMacrophagesMiceMicrogliaMultiple SclerosisPhosphoric Diester HydrolasesSignal TransductionSpinal CordCD11b Antigenlysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester Hydrolases

Identifiers

PMID32240164
PMCPMC7117669
OpenAlexW3014221166

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.