Evidence map›Paper›PMID 38969652›Full record

ArticleNature communications2024

Stage-specific GATA3 induction promotes ILC2 development after lineage commitment.

Hiroki Furuya, Yosuke Toda, Arifumi Iwata, Mizuki Kanai, Kodai Kato, Takashi Kumagai, Takahiro Kageyama, Shigeru Tanaka, Lisa Fujimura, Akemi Sakamoto and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2024. 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
–field-weighted citation impact
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.

  1. HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Peripheral SNCADiscover oncology · 2025
    Article
  10. Innate Lymphoid Cells Are the Rheostat of Immune Response in the Kidney.Journal of cellular and molecular medicine · 2025
    Review
  11. Review
  12. 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

14 authors.

Hiroki Furuya *Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-2288-923X
Yosuke Toda *Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Arifumi Iwata *Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan. aiwata@chiba-u.jp.ORCID 0000-0002-8771-481X
Mizuki KanaiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kodai KatoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takashi KumagaiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takahiro KageyamaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-9450-5848
Shigeru TanakaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-8466-110X
Lisa FujimuraBiomedical Research Center, Chiba University, Chiba, Japan.
Akemi SakamotoBiomedical Research Center, Chiba University, Chiba, Japan.
Masahiko HatanoBiomedical Research Center, Chiba University, Chiba, Japan.
Akira SutoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-2593-565X
Kotaro SuzukiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-4692-2970
Hiroshi NakajimaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan. nakajimh@faculty.chiba-u.jp.ORCID 0000-0001-8595-9381

Funding

Japan Agency for Medical Research and Development (AMED) 223fa627003h0002Japan Agency for Medical Research and Development (AMED) JP19ek0410043h0003MEXT | Japan Science and Technology Agency (JST) JPMJMS2025
6 · The paper itself

Abstract

Group 2 innate lymphoid cells (ILC2s) are a subset of innate lymphocytes that produce type 2 cytokines, including IL-4, IL-5, and IL-13. GATA3 is a critical transcription factor for ILC2 development at multiple stages. However, when and how GATA3 is induced to the levels required for ILC2 development remains unclear. Herein, we identify ILC2-specific GATA3-related tandem super-enhancers (G3SE) that induce high GATA3 in ILC2-committed precursors. G3SE-deficient mice exhibit ILC2 deficiency in the bone marrow, lung, liver, and small intestine with minimal impact on other ILC lineages or Th2 cells. Single-cell RNA-sequencing and subsequent flow cytometry analysis show that GATA3 induction mechanism, which is required for entering the ILC2 stage, is lost in IL-17RB

Indexed as

Cell LineageGATA3 Transcription FactorImmunity, InnateLymphocytesAnimalsCell DifferentiationEnhancer Elements, GeneticMiceMice, Inbred C57BLMice, KnockoutSingle-Cell AnalysisTh2 CellsGata3 protein, mouseGATA3 Transcription Factor

Identifiers

PMID38969652
PMCPMC11226602

What OpenQuestion holds

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Registered trials

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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.