Evidence map›Paper›PMID 30500858›Full record

ArticlePLoS pathogens2018

Ym1 induces RELMα and rescues IL-4Rα deficiency in lung repair during nematode infection.

Tara E Sutherland, Dominik Rückerl, Nicola Logan, Sheelagh Duncan, Thomas A Wynn, Judith E Allen

Abstract read
In one paragraph

Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Article
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  10. Macrophages: sentinels, warriors, and healers.Human molecular genetics · 2025
    Review
  11. Article
  12. Article
  13. Murine gut microbiota dysbiosis via enteric infection modulates the foreign body response to a distal biomaterial implant.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Article
  15. TIMD4JACC. Basic to translational science · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

6 authors.

Tara E SutherlandLydia Becker Institute for Immunology & Infection, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.ORCID 0000-0001-9334-8206
Dominik RückerlLydia Becker Institute for Immunology & Infection, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-0206-1451
Nicola LoganSchool of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom.
Sheelagh DuncanSchool of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0003-4397-4019
Thomas A WynnImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Judith E AllenLydia Becker Institute for Immunology & Infection, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-3829-066X

Funding

Medical Research Council MR/J001929/1Medical Research Council MR/K01207X/1Medical Research Council MR/K01207X/2MRF_ MRF-009-0002-RG-SUTHEWellcome TrustWellcome Trust 106898/A/15/Z
6 · The paper itself

Abstract

Ym1 and RELMα are established effector molecules closely synonymous with Th2-type inflammation and associated pathology. Here, we show that whilst largely dependent on IL-4Rα signaling during a type 2 response, Ym1 and RELMα also have IL-4Rα-independent expression patterns in the lung. Notably, we found that Ym1 has opposing effects on type 2 immunity during nematode infection depending on whether it is expressed at the time of innate or adaptive responses. During the lung migratory stage of Nippostrongylus brasiliensis, Ym1 promoted the subsequent reparative type 2 response but once that response was established, IL-4Rα-dependent Ym1 was important for limiting the magnitude of type 2 cytokine production from both CD4+ T cells and innate lymphoid cells in the lung. Importantly, our study demonstrates that delivery of Ym1 to IL-4Rα deficient animals drives RELMα production and overcomes lung repair deficits in mice deficient in type 2 immunity. Together, Ym1 and RELMα, exhibit time and dose-dependent interactions that determines the outcome of lung repair during nematode infection.

Indexed as

Animalsbeta-N-AcetylhexosaminidasesIntercellular Signaling Peptides and ProteinsInterleukin-4 Receptor alpha SubunitLectinsLungMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNematode InfectionsNippostrongylusReceptors, Cell SurfaceSignal TransductionStrongylida Infectionsbeta-N-AcetylhexosaminidasesChil3 protein, mouseIl4ra protein, mouseIntercellular Signaling Peptides and ProteinsInterleukin-4 Receptor alpha SubunitLectinsReceptors, Cell SurfaceRetnla protein, mouse

Identifiers

PMID30500858
PMCPMC6291165

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Registered trials

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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.