Evidence map›Paper›PMID 28898280›Full record

ArticlePloS one2017

ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection.

Pornpimon Angkasekwinai, Wichuda Sodthawon, Siranart Jeerawattanawart, Adithap Hansakon, Kovit Pattanapanyasat, Yui-Hsi Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  6. Critical and diverse role of alarmin cytokines in parasitic infections.Frontiers in cellular and infection microbiology · 2024
    Review
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  11. Review
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  13. Review
  14. Enteric Tuft Cells in Host-Parasite Interactions.Pathogens (Basel, Switzerland) · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. 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 at 3 institutions in 2 countries.

Pornpimon AngkasekwinaiDepartment of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani Thailand.ORCID http://orcid.org/0000-0003-0303-9544
Wichuda SodthawonDepartment of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani Thailand.
Siranart JeerawattanawartDepartment of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani Thailand.
Adithap HansakonDepartment of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani Thailand.
Kovit PattanapanyasatCenter of Excellence for Flow Cytometry, Office for Research and Development, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Yui-Hsi WangDivision of Allergy and Immunology, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, OH United States of America.
Thammasat University · THCincinnati Children's Hospital Medical Center · USSiriraj Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection.

Indexed as

AnimalsCells, CulturedGenes, MHC Class IIGoblet CellsImmunity, InnateInterleukin-10Interleukin-17InterleukinsMast CellsMiceMice, Inbred BALB CReceptors, Interleukin-17Th2 CellsTrichinella spiralisTrichinellosisIl17rb protein, mouseIl19 protein, mouseInterleukin-10Interleukin-17InterleukinsReceptors, Interleukin-17

Identifiers

PMID28898280
PMCPMC5595335
OpenAlexW2755583791

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.