Evidence map›Paper›PMID 38182668›Full record

ArticleNature immunology2024

IKAROS and AIOLOS directly regulate AP-1 transcriptional complexes and are essential for NK cell development.

Wilford Goh, Harrison Sudholz, Momeneh Foroutan, Sebastian Scheer, Aline Pfefferle, Rebecca B Delconte, Xiangpeng Meng, Zihan Shen, Robert Hennessey, Isabella Y Kong and 15 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  8. Article
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  10. Review
  11. Rescuing natural killer cells from the cancer wilderness.Journal for immunotherapy of cancer · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. A new pipeline SPICE identifies novel JUN-IKZF1 composite elements.bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. 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

25 authors at 6 institutions in 3 countries.

Wilford Goh *The Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.
Harrison Sudholz *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0009-0000-6848-4230
Momeneh Foroutan *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-1440-0457
Sebastian Scheer *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-9716-5009
Aline Pfefferle *Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-8181-537X
Rebecca B DelconteThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.
Xiangpeng MengDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Zihan ShenDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Robert HennesseyThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.
Isabella Y KongThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.
Iona S SchusterInfection and Immunity Program and Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Christopher E AndoniouInfection and Immunity Program and Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0003-0566-3180
Melissa J DavisThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0003-4864-7033
Soroor Hediyeh-ZadehThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0001-7513-6779
Fernando Souza-Fonseca-GuimaraesFrazer Institute, University of Queensland, Woolloongabba, Queensland, Australia.ORCID http://orcid.org/0000-0002-2037-8946
Ian A ParishCancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0003-3528-478X
Paul BeavisCancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0002-2116-013X
Daniel ThieleDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-4469-8215
Michael ChopinDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Mariapia A Degli-EspostiInfection and Immunity Program and Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Joe CursonsDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-5053-4540
Axel KalliesDepartment of Microbiology & Immunology, Faculty of Medicine, Dentistry and Health Sciences & Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0002-6312-6968
Jai RautelaDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.ORCID http://orcid.org/0000-0002-4253-9966
Stephen L NuttThe Walter and Eliza Hall Institute of Medical Research. Department of Medical Biology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0002-0020-6637
Nicholas D HuntingtonDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia. nicholas.huntington@monash.edu.ORCID http://orcid.org/0000-0002-5267-7211
Australian Regenerative Medicine Institute · AUThe University of Melbourne · AULions Eye Institute · AUThe University of Queensland · AUDiscovery Institute · USMemorial Sloan Kettering Cancer Center · US

Funding

Department of Health | National Health and Medical Research Council (NHMRC) 1124784Department of Health | National Health and Medical Research Council (NHMRC) 1195296
6 · The paper itself

Abstract

Ikaros transcription factors are essential for adaptive lymphocyte function, yet their role in innate lymphopoiesis is unknown. Using conditional genetic inactivation, we show that Ikzf1/Ikaros is essential for normal natural killer (NK) cell lymphopoiesis and IKZF1 directly represses Cish, a negative regulator of interleukin-15 receptor resulting in impaired interleukin-15 receptor signaling. Both Bcl2l11 and BIM levels, and intrinsic apoptosis were increased in Ikzf1-null NK cells, which in part accounts for NK lymphopenia as both were restored to normal levels when Ikzf1 and Bcl2l11 were co-deleted. Ikzf1-null NK cells presented extensive transcriptional alterations with reduced AP-1 transcriptional complex expression and increased expression of Ikzf2/Helios and Ikzf3/Aiolos. IKZF1 and IKZF3 directly bound AP-1 family members and deletion of both Ikzf1 and Ikzf3 in NK cells resulted in further reductions in Jun/Fos expression and complete loss of peripheral NK cells. Collectively, we show that Ikaros family members are important regulators of apoptosis, cytokine responsiveness and AP-1 transcriptional activity.

Indexed as

Killer Cells, NaturalTranscription Factor AP-1Ikaros Transcription FactorReceptors, Interleukin-15Ikaros Transcription FactorReceptors, Interleukin-15Transcription Factor AP-1

Identifiers

PMID38182668
OpenAlexW4390616148

What OpenQuestion holds

Textmetadata
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.