Evidence map›Paper›PMID 32103032›Full record

ArticleScientific reports2020

p38 MAPK signalling regulates cytokine production in IL-33 stimulated Type 2 Innate Lymphoid cells.

Tsvetana Petrova, Jelena Pesic, Katerina Pardali, Matthias Gaestel, J Simon C Arthur

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Berberine Inhibits Eczematous SkinInternational journal of molecular sciences · 2026
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  12. Lung-resident lymphocytes and their roles in respiratory infections and chronic respiratory diseases.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
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  14. Article
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  18. Sensitization of colonic nociceptors by IL-13 is dependent on JAK and p38 MAPK activity.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  19. Article
  20. 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 3 institutions in 3 countries.

Tsvetana PetrovaDivision of Cell Signalling and Immunology, School of Life Sciences, Wellcome Trust Building, University of Dundee, Dundee, DD1 5EH, UK.ORCID http://orcid.org/0000-0003-2425-2459
Jelena PesicRespiratory, Inflammation & Autoimmunity IMED Biotech Unit, AstraZeneca, Gothenburg, Mölndal, 43183, Sweden.
Katerina PardaliRespiratory, Inflammation & Autoimmunity IMED Biotech Unit, AstraZeneca, Gothenburg, Mölndal, 43183, Sweden.
Matthias GaestelInstitute for Cell Biochemistry, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover, 30623, Germany.ORCID http://orcid.org/0000-0002-4944-4652
J Simon C ArthurDivision of Cell Signalling and Immunology, School of Life Sciences, Wellcome Trust Building, University of Dundee, Dundee, DD1 5EH, UK. j.s.c.arthur@dundee.ac.uk.
AstraZeneca (Sweden) · SEUniversity of Dundee · GBMedizinische Hochschule Hannover · DE

Funding

RCUK | Medical Research Council (MRC) MR/L008785/1Wellcome TrustWellcome Trust (Wellcome) 102132/Z/13/Z
6 · The paper itself

Abstract

Type 2 Innate lymphoid cells (ILC2s) are implicated in helminth infections and asthma where they play a role in the production of Th2-type cytokines. ILC2s express the IL-33 receptor and are a major cell type thought to mediate the effects of this cytokine in vivo. To study the signalling pathways that mediate IL-33 induced cytokine production, a culture system was set up to obtain pure populations of ILC2s from mice. Inhibitors of the p38α/β and ERK1/2 MAPK pathways reduced the production of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, with inhibition of p38 having the greatest effect. MK2 and 3 are kinases activated by p38α; MK2/3 inhibitors or knockout of MK2/3 in mice reduced the production of IL-6 and IL-13 (two cytokines implicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33. MK2/3 inhibition also suppressed IL-6 and IL-13 production by human ILC2s. MK2/3 were required for maximal S6 phosphorylation, suggesting an input from the p38α-MK2/3 pathway to mTOR1 activation in ILC2s. The mTORC1 inhibitor rapamycin also reduced IL-6 and IL-13 production, which would be consistent with a model in which MK2/3 regulate IL-6 and IL-13 via mTORC1 activation in ILC2s.

Indexed as

AnimalsCells, CulturedCytokinesDown-RegulationHumansInterleukin-13Interleukin-33Interleukin-6Intracellular Signaling Peptides and ProteinsLymphocytesMAP-Kinase-Activated Kinase 2MAP Kinase Signaling SystemMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutCytokinesInterleukin-13Interleukin-33Interleukin-6Intracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MAP-kinase-activated kinase 3Mechanistic Target of Rapamycin Complex 1p38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProtein Serine-Threonine KinasesSirolimus

Identifiers

PMID32103032
PMCPMC7044202
OpenAlexW3007795315

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.