Evidence map›Paper›PMID 27581382›Full record

ArticleNature communications2016

Bach2-Batf interactions control Th2-type immune response by regulating the IL-4 amplification loop.

Makoto Kuwahara, Wataru Ise, Mizuki Ochi, Junpei Suzuki, Kohei Kometani, Saho Maruyama, Maya Izumoto, Akira Matsumoto, Nobuaki Takemori, Ayako Takemori and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
6.0field-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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. BACH2 the future.Nature immunology · 2026
    Article
  5. Review
  6. Inborn errors of regulatory T-cell differentiation and function.The Journal of allergy and clinical immunology · 2025
    Review
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  8. Article
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  11. Review
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  18. Review
  19. Article
  20. Article

6 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

17 authors at 7 institutions in 1 country.

Makoto KuwaharaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Wataru IseDepartment of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Mizuki OchiDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Junpei SuzukiDepartment of Translational Immunology, Translational Research Center, Ehime University Hospital, Shitsukawa, Toon, Ehime 791-0295, Japan.
Kohei KometaniLaboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences, 1-7-22 suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan.
Saho MaruyamaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Maya IzumotoDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Akira MatsumotoDepartment of Infection and Host Defenses, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Nobuaki TakemoriDivision of Proteomics, Department of Proteo-Medicine, Proteo-Science Center, Ehime University, Toon, Ehime 791-0295, Japan.
Ayako TakemoriDivision of Proteomics, Department of Proteo-Medicine, Proteo-Science Center, Ehime University, Toon, Ehime 791-0295, Japan.
Kenta ShinodaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670 Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670 Japan.
Osamu OharaHuman DNA Analysis Group, Department of Technology Development, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 292-0818, Japan.ORCID http://orcid.org/0000-0002-3328-9571
Masaki YasukawaDepartment of Hematology, Clinical Immunology and Infectious Diseases, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Tatsuya SawasakiDivision of Cell-Free Sciences, Department of Proteo-Research, Proteo-Science Center, Ehime University, Matsuyama, Ehime 790-8577, Japan.
Tomohiro KurosakiDepartment of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Masakatsu YamashitaDepartment of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime 791-0295, Japan.
Ehime University · JPEhime University Hospital · JPChiba University · JPRIKEN Center for Integrative Medical Sciences · JPCellFree Sciences (Japan) · JPKazusa DNA Research Institute · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Bach2 has an important role in regulating the Th2-type immune response, the underlying molecular mechanisms remain unclear. We herein demonstrate that Bach2 associates with Batf and binds to the regulatory regions of the Th2 cytokine gene loci. The Bach2-Batf complex antagonizes the recruitment of the Batf-Irf4 complex to AP-1 motifs and suppresses Th2 cytokine production. Furthermore, we find that Bach2 regulates the Batf and Batf3 expressions via two distinct pathways. First, Bach2 suppresses the maintenance of the Batf and Batf3 expression through the inhibition of IL-4 production. Second, the Bach2-Batf complex directly binds to the Batf and Batf3 gene loci and reduces transcription by interfering with the Batf-Irf4 complex. These findings suggest that IL-4 and Batf form a positive feedback amplification loop to induce Th2 cell differentiation and the subsequent Th2-type immune response, and Bach2-Batf interactions are required to prevent an excessive Th2 response.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsCell DifferentiationFemaleGene Expression RegulationInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-4MaleMiceMice, Inbred C57BLMice, KnockoutRepressor ProteinsSTAT6 Transcription FactorTh2 CellsTranscription, GeneticBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsBatf protein, mouseInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-4Repressor ProteinsSNFT protein, mouseStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID27581382
PMCPMC5025763
OpenAlexW2514911561

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.