Evidence map›Paper›PMID 27421703›Full record

ArticleImmunity2016

Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis.

Richard L Gieseck, Thirumalai R Ramalingam, Kevin M Hart, Kevin M Vannella, David A Cantu, Wei-Yu Lu, Sofía Ferreira-González, Stuart J Forbes, Ludovic Vallier, Thomas A Wynn

Open access · greenAbstract read
In one paragraph

Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  15. Article
  16. Generation and repair of thymic epithelial cells.The Journal of experimental medicine · 2024
    Review
  17. Review
  18. Global IL4Rα blockade exacerbates heart failure after an ischemic event in mice and humans.American journal of physiology. Heart and circulatory physiology · 2024
    Observational
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 2 countries.

Richard L GieseckImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA; Wellcome Trust-Medical Research Council Stem Cell Institute, Anne McLaren Laboratory, Department of Surgery, University of Cambridge, Cambridge CB2 0SZ, UK.
Thirumalai R RamalingamImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA.
Kevin M HartImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA.
Kevin M VannellaImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA.
David A CantuImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA.
Wei-Yu LuMedical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK.
Sofía Ferreira-GonzálezMedical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK.
Stuart J ForbesMedical Research Council Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH16 4UU, UK.
Ludovic VallierWellcome Trust-Medical Research Council Stem Cell Institute, Anne McLaren Laboratory, Department of Surgery, University of Cambridge, Cambridge CB2 0SZ, UK; Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.
Thomas A WynnImmunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20852, USA. Electronic address: twynn@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USUniversity of Edinburgh · GBMedical Research Council · GBMRC Centre for Regenerative Medicine · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
Mechanisms of Fibrosis in Asthma and Other Fibroproliferative DiseasesZIAAI001019 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$7.1M
Immunological Intervention In SchistosomiasisZ01AI000829 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI WYNN, THOMAS · 1998 to 2008
$3.4M
Mechanisms of Fibrosis in Asthma and Other Fibroproliferative DiseasesZ01AI001019 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI WYNN, THOMAS · 2007 to 2008
$635k
Department of HealthIntramural NIH HHS Z01 AI000829Intramural NIH HHS Z01 AI001019Medical Research Council MC_PC_12009Medical Research Council MR/K017047/1Medical Research Council MR/K026666/1
6 · The paper itself

Abstract

Fibroproliferative diseases are driven by dysregulated tissue repair responses and are a major cause of morbidity and mortality because they affect nearly every organ system. Type 2 cytokine responses are critically involved in tissue repair; however, the mechanisms that regulate beneficial regeneration versus pathological fibrosis are not well understood. Here, we have shown that the type 2 effector cytokine interleukin-13 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease induced by interleukin-13 overexpression or after infection with Schistosoma mansoni. Using transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction. Together, these studies show that these mechanisms are simultaneously controlled but distinctly regulated by interleukin-13 signaling. Thus, it may be possible to promote interleukin-13-dependent hepatobiliary expansion without generating pathological fibrosis. VIDEO ABSTRACT.

Indexed as

AnimalsBile Acids and SaltsCell ProliferationCells, CulturedFatty LiverFibroblastsFibrosisHumansInterleukin-13LiverLiver Cirrhosis, BiliaryMiceMice, Inbred C57BLMice, KnockoutSchistosoma mansoniSchistosomiasis mansoniBile Acids and SaltsInterleukin-13

Identifiers

PMID27421703
PMCPMC4956513
OpenAlexW2472778407

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.