Evidence map›Paper›PMID 29018331›Full record

ArticleFrontiers in cellular neuroscience2017

Distinctive Roles for α7*- and α9*-Nicotinic Acetylcholine Receptors in Inflammatory and Autoimmune Responses in the Murine Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.

Qiang Liu, Paul Whiteaker, Barbara J Morley, Fu-Dong Shi, Ronald J Lukas

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Phytochemicals derived fromFrontiers in pharmacology · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Immune and autonomic nervous system interactions in multiple sclerosis: clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Qiang LiuDivision of Neurobiology, Barrow Neurological InstitutePhoenix, AZ, United States.
Paul WhiteakerDivision of Neurobiology, Barrow Neurological InstitutePhoenix, AZ, United States.
Barbara J MorleyBoys Town National Research HospitalOmaha, NE, United States.
Fu-Dong ShiDivision of Neurobiology, Barrow Neurological InstitutePhoenix, AZ, United States.
Ronald J LukasDivision of Neurobiology, Barrow Neurological InstitutePhoenix, AZ, United States.
Barrow Neurological Institute · USBoys Town National Research Hospital · US

Funding

Alpha9*-Nicotinic Receptors in Autoimmunity and InflammationR21NS082902 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI LUKAS, RONALD JOHN · 2013 to 2014
$423k
NINDS NIH HHS R21 NS082902
6 · The paper itself

Abstract

Previous studies have demonstrated immunosuppressive and anti-inflammatory effects of nicotine, including in the experimental autoimmune encephalomyelitis (EAE) model in mice of some forms of multiple sclerosis (MS). Other studies using knock-out (KO) mice have implicated nicotinic acetylcholine (ACh) receptors containing α7, α9, or β2 subunits (α7*-, α9*- or β2*-nAChR) in different, disease-exacerbating or disease-ameliorating processes. These outcomes are in harmony with gene expression analyses showing nAChR subunit mRNA in many classes of immune system cell types. Consistent with influences on disease status, predictable effects of nAChR subunit (and subtype) KO, or of nicotine exposure, are seen on immune cell numbers and distribution and on cytokine levels or other markers of immunity, inflammation, demyelination, and axonal degradation. Providing support for our hypotheses about distinctive roles for nAChR subtypes in EAE, here we have used direct and adoptive EAE induction and a nAChR subunit gene double knock-out (DKO) strategy. Immune cell expression of nAChR α9 subunits as protein is demonstrated by immunostaining of isolated CD4

Indexed as

auto-immunitycholinergic anti-inflammatory pathwayexperimental autoimmune encephalomyelitisinflammationmultiple sclerosisnicotinic acetylcholine receptors

Identifiers

PMID29018331
PMCPMC5615207
OpenAlexW2757434377

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.