Evidence map›Paper›PMID 29758102›Full record

ArticleImmunology and cell biology2018

Purine metabolism controls innate lymphoid cell function and protects against intestinal injury.

Siobhan Crittenden, Ashleigh Cheyne, Alexander Adams, Thorsten Forster, Calum T Robb, Jennifer Felton, Gwo-Tzer Ho, Dominik Ruckerl, Adriano G Rossi, Stephen M Anderton and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Immunology and cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Anti-inflammatory activity of Chlorella polysaccharide AHP.Molecular and cellular biochemistry · 2026
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  13. Investigation ofMetabolites · 2024
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  18. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  19. Review
  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

14 authors at 5 institutions in 1 country.

Siobhan CrittendenMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Ashleigh CheyneMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Alexander AdamsGastrointestinal Unit, Institute of Genetics and Molecular Medicine, Western General Hospital, The University of Edinburgh, Edinburgh, EH4 2XU, UK.
Thorsten ForsterDivision of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh, EH16 4SB, UK.
Calum T RobbMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Jennifer FeltonMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Gwo-Tzer HoMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Dominik RuckerlFaculty of Biology, Medicine and Health, School of Biological Sciences, The University of Manchester, Manchester, M13 9PT, UK.
Adriano G RossiMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Stephen M AndertonMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Peter GhazalDivision of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh, EH16 4SB, UK.
Jack SatsangiGastrointestinal Unit, Institute of Genetics and Molecular Medicine, Western General Hospital, The University of Edinburgh, Edinburgh, EH4 2XU, UK.
Sarah E HowieMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Chengcan YaoMedical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, EH16 4TJ, UK.
University of Edinburgh · GBCentre for Inflammation Research · GBMedical Research Council · GBUniversity of Manchester · GBWestern General Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council BB/K091121/1Cancer Research UK 25246Cancer Research UK C63480/A25246Chief Scientist Office ETM/202Medical Research Council G0601481Medical Research Council G0701898Medical Research Council G0801924Medical Research Council G0901697Medical Research Council MR/K013386/1Medical Research Council MR/R008167/1Wellcome Trust
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a condition of chronic inflammatory intestinal disorder with increasing prevalence but limited effective therapies. The purine metabolic pathway is involved in various inflammatory processes including IBD. However, the mechanisms through which purine metabolism modulates IBD remain to be established. Here, we found that mucosal expression of genes involved in the purine metabolic pathway is altered in patients with active ulcerative colitis (UC), which is associated with elevated gene expression signatures of the group 3 innate lymphoid cell (ILC3)-interleukin (IL)-22 pathway. In mice, blockade of ectonucleotidases (NTPDases), critical enzymes for purine metabolism by hydrolysis of extracellular adenosine 5'-triphosphate (eATP) into adenosine, exacerbates dextran-sulfate sodium-induced intestinal injury. This exacerbation of colitis is associated with reduction of colonic IL-22-producing ILC3s, which afford essential protection against intestinal inflammation, and is rescued by exogenous IL-22. Mechanistically, activation of ILC3s for IL-22 production is reciprocally mediated by eATP and adenosine. These findings reveal that the NTPDase-mediated balance between eATP and adenosine regulates ILC3 cell function to provide protection against intestinal injury and suggest potential therapeutic strategies for treating IBD by targeting the purine-ILC3 axis.

Indexed as

Immunity, InnateAnimalsBiomarkersColitisDextran SulfateDisease Models, AnimalFlow CytometryGene Expression ProfilingIntestinal MucosaLymphocytesMiceMice, KnockoutPurinesTranscriptomeBiomarkersDextran SulfatePurinesAdenosineectonucleotidase (NTPDase)IL-22intestinal injurypurinergic signalingtype 3 innate lymphoid cell (ILC3)

Identifiers

PMID29758102
PMCPMC6248310
OpenAlexW2804157958

What OpenQuestion holds

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Read underepoch 390

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.