Evidence map›Paper›PMID 29540770›Full record

ArticleScientific reports2018

IL-33/ST2 signalling and crosstalk with FcεRI and TLR4 is targeted by the parasitic worm product, ES-62.

Dimity H Ball, Lamyaa Al-Riyami, William Harnett, Margaret M Harnett

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
17.7field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Modulation of the Immune Response by Nematode Derived Molecules.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Interference of LPSCells · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Frontiers in immunology · 2020
    Review
  16. Review
  17. The IL-33/sST2 Axis in Thromboangiitis Obliterans.Journal of inflammation research · 2020
    Article
  18. Review
  19. Review
  20. Interleukin-33: Its Emerging Role in Allergic Diseases.Molecules (Basel, Switzerland) · 2018
    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

4 authors at 3 institutions in 1 country.

Dimity H BallInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8TA, Scotland.
Lamyaa Al-RiyamiStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, G4 0RE, Scotland.
William HarnettStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, G4 0RE, Scotland.
Margaret M HarnettInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8TA, Scotland. Margaret.Harnett@glasgow.ac.uk.ORCID 0000-0001-5740-3028
University of Strathclyde · GBUniversity of Glasgow · GBWellcome Centre for Molecular Parasitology · GB

Funding

Medical Research CouncilWellcome TrustWellcome Trust 086852
6 · The paper itself

Abstract

ES-62 is a secreted parasitic worm-derived immunomodulator that exhibits therapeutic potential in allergy by downregulating aberrant MyD88 signalling to normalise the inflammatory phenotype and mast cell responses. IL-33 plays an important role in driving mast cell responses and promoting type-2 allergic inflammation, particularly with respect to asthma, via MyD88-integrated crosstalk amongst the IL-33 receptor (ST2), TLR4 and FcεRI. We have now investigated whether ES-62 targets this pathogenic network by subverting ST2-signalling, specifically by characterising how the functional outcomes of crosstalk amongst ST2, TLR4 and FcεRI are modulated by the worm product in wild type and ST2-deficient mast cells. This analysis showed that whilst ES-62 inhibits IL-33/ST2 signalling, the precise functional modulation observed varies with receptor usage and/or mast cell phenotype. Thus, whilst ES-62's harnessing of the capacity of ST2 to sequester MyD88 appears sufficient to mediate its inhibitory effects in peritoneal-derived serosal mast cells, downregulation of MyD88 expression appears to be required to dampen the higher levels of cytokine production typically released by bone marrow-derived mucosal mast cells.

Indexed as

AnimalsCell DegranulationCytokinesHelminth ProteinsImmunomodulationInflammation MediatorsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Mast CellsMiceMice, KnockoutProtein BindingReceptors, IgESignal TransductionToll-Like Receptor 4CytokinesES-62 protein, Acanthocheilonema viteaeHelminth ProteinsIl1rl1 protein, mouseInflammation MediatorsInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Receptors, IgEToll-Like Receptor 4

Identifiers

PMID29540770
PMCPMC5852134
OpenAlexW2793153047

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.