Evidence map›Paper›PMID 29470558›Full record

ArticlePLoS pathogens2018

HIC1 links retinoic acid signalling to group 3 innate lymphoid cell-dependent regulation of intestinal immunity and homeostasis.

Kyle Burrows, Frann Antignano, Alistair Chenery, Michael Bramhall, Vladimir Korinek, T Michael Underhill, Colby Zaph

Open access · goldAbstract 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 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  4. Review
  5. Review
  6. Insights into phenotypic and functional CD8Immunological reviews · 2023
    Review
  7. Article
  8. Innate Lymphoid Cells and Inflammatory Bowel Disease.Advances in experimental medicine and biology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. 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

7 authors at 3 institutions in 3 countries.

Kyle BurrowsThe Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.ORCID 0000-0001-5371-3512
Frann AntignanoThe Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
Alistair CheneryThe Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.ORCID 0000-0001-8755-461X
Michael BramhallInfection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID 0000-0001-5938-158X
Vladimir KorinekDepartment of Cell and Developmental Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
T Michael UnderhillThe Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.
Colby ZaphThe Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada.ORCID 0000-0002-9889-9848
University of British Columbia · CAAustralian Regenerative Medicine Institute · AUCzech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intestinal immune system must be able to respond to a wide variety of infectious organisms while maintaining tolerance to non-pathogenic microbes and food antigens. The Vitamin A metabolite all-trans-retinoic acid (atRA) has been implicated in the regulation of this balance, partially by regulating innate lymphoid cell (ILC) responses in the intestine. However, the molecular mechanisms of atRA-dependent intestinal immunity and homeostasis remain elusive. Here we define a role for the transcriptional repressor Hypermethylated in cancer 1 (HIC1, ZBTB29) in the regulation of ILC responses in the intestine. Intestinal ILCs express HIC1 in a vitamin A-dependent manner. In the absence of HIC1, group 3 ILCs (ILC3s) that produce IL-22 are lost, resulting in increased susceptibility to infection with the bacterial pathogen Citrobacter rodentium. Thus, atRA-dependent expression of HIC1 in ILC3s regulates intestinal homeostasis and protective immunity.

Indexed as

Immunity, InnateAnimalsCitrobacter rodentiumEnterobacteriaceae InfectionsGene Expression RegulationHomeostasisIntestinesKruppel-Like Transcription FactorsLymphocytesMiceMice, Inbred C57BLMice, TransgenicSignal TransductionTretinoinHic1 protein, mouseKruppel-Like Transcription FactorsTretinoin

Identifiers

PMID29470558
PMCPMC5823476
OpenAlexW2953155429

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.