Evidence map›Paper›PMID 25249168›Full record

ArticleMucosal immunology2015

Reciprocal regulation of lymphoid tissue development in the large intestine by IL-25 and IL-23.

D S Donaldson, B M Bradford, D Artis, N A Mabbott

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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  12. A missense variant inProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Review
  14. Article
  15. Microbiome Influence in the Pathogenesis of Prion and Alzheimer's Diseases.International journal of molecular sciences · 2019
    Review
  16. Article
  17. Article
  18. Effect of Homocysteine on the Differentiation of CD4Digestive diseases and sciences · 2018
    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

4 authors at 3 institutions in 2 countries.

D S DonaldsonThe Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, UK.
B M BradfordThe Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, UK.
D ArtisDepartment of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
N A MabbottThe Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, UK.
University of Edinburgh · GBRoslin Institute · GBUniversity of Pennsylvania · US

Funding

Biotechnology and Biological Sciences Research Council BB/G003947/1Biotechnology and Biological Sciences Research Council BB/I001107/1Biotechnology and Biological Sciences Research Council BBS/E/D/20251967Biotechnology and Biological Sciences Research Council BBS/E/D/20251968
6 · The paper itself

Abstract

Isolated lymphoid follicles (ILFs) develop after birth in the small and large intestines (SI and LI) and represent a dynamic response of the gut immune system to the microbiota. Despite their similarities, ILF development in the SI and LI differs on a number of levels. We show that unlike ILF in the SI, the microbiota inhibits ILF development in the colon as conventionalization of germ-free mice reduced colonic ILFs. From this, we identified a novel mechanism regulating colonic ILF development through the action of interleukin (IL)-25 on IL-23 and its ability to modulate T regulatory cell (Treg) differentiation. Colonic ILF develop in the absence of a number of factors required for the development of their SI counterparts and can be specifically suppressed by factors other than IL-25. However, IL-23 is the only factor identified that specifically promotes colonic ILFs without affecting SI-ILF development. Both IL-23 and ILFs are associated with inflammatory bowel disease, suggesting that disruption to this pathway may have an important role in the breakdown of microbiota-immune homeostasis.

Indexed as

AnimalsB-LymphocytesDisease Models, AnimalGene Expression RegulationInflammatory Bowel DiseasesInterleukin-23InterleukinsIntestine, LargeIntestine, SmallLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutPeyer's PatchesSignal TransductionInterleukin-23InterleukinsMydgf protein, mouse

Identifiers

PMID25249168
PMCPMC4424384
OpenAlexW2077966865

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.