Evidence map›Paper›PMID 23800789›Full record

ArticleCytokine2013

The IL17A and IL17F loci have divergent histone modifications and are differentially regulated by prostaglandin E2 in Th17 cells.

Juraj Adamik, Matthew Henkel, Anuradha Ray, Philip E Auron, Richard Duerr, Arthur Barrie

Abstract read
In one paragraph

Article in Cytokine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. PD-L1 up-regulation restrains Th17 cell differentiation inThe Journal of experimental medicine · 2017
    Article
  8. Abnormal CD161The Journal of allergy and clinical immunology · 2017
    Article
  9. Article
  10. Role of Fas and Treg cells in fracture healing as characterized in the fas-deficient (lpr) mouse model of lupus.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Article
  11. Review
  12. Mucosal healing and deep remission: what does it mean?World journal of gastroenterology · 2013
    Review
  13. Review
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 2 institutions in 1 country.

Juraj AdamikDepartment of Biological Sciences, Duquesne University, Pittsburgh, PA 15282, USA.
Matthew Henkel
Anuradha Ray
Philip E Auron
Richard Duerr
Arthur Barrie
University of Pittsburgh · USDuquesne University · US

Funding

University of Pittsburgh Clinical and Translational Science InstitutionKL2RR024154 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2006 to 2011
$22.2M
University of Pittsburgh Clinical and Translational Science InstitutionKL2TR000146 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$8.7M
NIDDK IBD Genetics Consortium Genetic Research CenterU01DK062420 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DUERR, RICHARD H · 2002 to 2021
$7.8M
Intramural NIH HHSNCATS NIH HHS KL2 TR000146NCRR NIH HHS KL2 RR024154NIDDK NIH HHS U01 DK062420
6 · The paper itself

Abstract

Prostaglandin E2 (PGE2), IL-23 and IL-1β are implicated in inflammatory bowel disease susceptibility, likely in part by modulating IL-17 producing CD4(+) T helper (Th17) cells. To better understand how these three mediators affect Th17 cell memory responses, we characterized the gene expression profiles of activated human peripheral CD4(+) effector memory T cells and sorted Th17 memory cells from healthy donors concurrent with IL17A mRNA induction mediated by PGE2 and/or IL-23 plus IL-1β. We discovered that PGE2 and IL-23 plus IL-1β differentially regulate Th17 cytokine expression and synergize to induce IL-17A, but not IL-17F. IL-23 plus IL-1β preferentially induce IL-17F expression. The addition of PGE2 to IL-23 plus IL-1β only enhances IL-17A expression as mediated by the PGE2 EP4 receptor, and promotes a switch from an IL-17F to an IL-17A predominant immune response. The human Th17 HuT-102 cell line was also found to constitutively express IL-17A, but not IL-17F. We went on to show that the IL17A and IL17F loci have divergent epigenetic architectures in unstimulated HuT-102 and primary Th17 cells and are poised for preferential expression of IL17A. We conclude that the chromatin for IL17A and IL17F are distinctly regulated, which may play an important role in mucosal health and disease.

Indexed as

Cell LineChromatinCyclic AMPHistonesHumansImmunologic MemoryInterleukin-17Interleukin-1betaInterleukin-23Prostaglandins EReceptors, Prostaglandin E, EP4 SubtypeRNA, MessengerSignal TransductionTh17 CellsChromatinCyclic AMPHistonesIL17A protein, humanIL17F protein, humanInterleukin-17Interleukin-1betaInterleukin-23Prostaglandins EReceptors, Prostaglandin E, EP4 SubtypeRNA, Messenger1-hydroxy prostaglandin E11-OH-PGE1ChIPChromatinchromatin immunoprecipitationC(T)EPE prostanoidgenome wide association studiesGWASIBDIL-17AIL-17Finflammatory bowel diseasePGE2prostaglandin E2Prostaglandin E2ThTh17T helperthreshold cycle

Identifiers

PMID23800789
PMCPMC3770803
OpenAlexW2052415979

What OpenQuestion holds

Textmetadata
LicenceTDM
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.