Evidence map›Paper›PMID 27438771›Full record

ArticleImmunity2016

Ikaros Inhibits Group 3 Innate Lymphoid Cell Development and Function by Suppressing the Aryl Hydrocarbon Receptor Pathway.

Shiyang Li, Jennifer J Heller, John W Bostick, Aileen Lee, Hilde Schjerven, Philippe Kastner, Susan Chan, Zongming E Chen, Liang Zhou

Open access · bronzeAbstract 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026
    Review
  2. Mediators of inflammation · 2026
    Article
  3. Review
  4. iScience · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Transcriptional control of ILC identity.Frontiers in immunology · 2023
    Review
  9. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
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  20. 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

9 authors at 6 institutions in 2 countries.

Shiyang LiDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA.
Jennifer J HellerDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
John W BostickDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Chemical and Biological Engineering, McCormick School of Engineering, Northwestern University, Evanston, IL 60208, USA.
Aileen LeeDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Hilde SchjervenDepartment of Laboratory Medicine, UCSF School of Medicine, San Francisco, CA 94143, USA.
Philippe KastnerInstitut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM U964, CNRS UMR 7104, Université de Strasbourg, 67404 Illkirch, France.
Susan ChanInstitut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM U964, CNRS UMR 7104, Université de Strasbourg, 67404 Illkirch, France.
Zongming E ChenDepartment of Laboratory Medicine in Geisinger Health System, 100 N. Academy Avenue, MC 19-20, Danville, PA 17822, USA.
Liang ZhouDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. Electronic address: liangzhou497@ufl.edu.
Northwestern University · USCentre National de la Recherche Scientifique · FRGeisinger Health System · USInserm · FRUniversity of California, San Francisco · USUniversity of Florida · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
AhR activation in Th17 and Treg cell differentiationR01AI089954 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ZHOU, LIANG · 2010 to 2014
$1.9M
ROLE OF AHR IN T LYMPHOCYTE DEVELOPMENT AND FUNCTIONR01DK105562 · NIDDK · UNIVERSITY OF FLORIDA · PI ZHOU, LIANG · 2015 to 2019
$1.8M
NCI NIH HHS P30 CA060553NIAID NIH HHS R01 AI089954NIDDK NIH HHS R01 DK105562
6 · The paper itself

Abstract

Group 3 innate lymphoid cells (ILC3s) expressing the transcription factor (TF) RORγt are important for the defense and homeostasis of host intestinal tissues. The zinc finger TF Ikaros, encoded by Ikzf1, is essential for the development of RORγt(+) fetal lymphoid tissue inducer (LTi) cells and lymphoid organogenesis, but its role in postnatal ILC3s is unknown. Here, we show that small-intestinal ILC3s had lower Ikaros expression than ILC precursors and other ILC subsets. Ikaros inhibited ILC3s in a cell-intrinsic manner through zinc-finger-dependent inhibition of transcriptional activity of the aryl hydrocarbon receptor, a key regulator of ILC3 maintenance and function. Ablation of Ikzf1 in RORγt(+) ILC3s resulted in increased expansion and cytokine production of intestinal ILC3s and protection against infection and colitis. Therefore, in contrast to being required for LTi development, Ikaros inhibits postnatal ILC3 development and function to regulate gut immune responses at steady state and in disease.

Indexed as

AnimalsCell DifferentiationCells, CulturedColitisDextran SulfateHomeostasisIkaros Transcription FactorImmunity, InnateIntestinal MucosaLymphocyte ActivationLymphocytesMiceMice, Inbred C57BLMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl HydrocarbonDextran SulfateIkaros Transcription FactorNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl HydrocarbonZfpn1a1 protein, mouse

Identifiers

PMID27438771
PMCPMC4959810
OpenAlexW2491658239

What OpenQuestion holds

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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.