Evidence map›Paper›PMID 30911105›Full record

ArticleNature immunology2019

Safeguard function of PU.1 shapes the inflammatory epigenome of neutrophils.

Josephine Fischer, Carolin Walter, Alexander Tönges, Hanna Aleth, Marta Joana Costa Jordão, Mathias Leddin, Verena Gröning, Tabea Erdmann, Georg Lenz, Johannes Roth and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. MMP9Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
  7. ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 2 countries.

Josephine FischerInstitute of Molecular Tumor Biology, University of Muenster, Muenster, Germany.ORCID http://orcid.org/0000-0003-3773-9311
Carolin WalterInstitute of Medical Informatics, University of Muenster, Muenster, Germany.
Alexander TöngesInstitute of Molecular Tumor Biology, University of Muenster, Muenster, Germany.
Hanna AlethInstitute of Molecular Tumor Biology, University of Muenster, Muenster, Germany.
Marta Joana Costa JordãoInstitute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0001-7888-2195
Mathias LeddinMax-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Verena GröningInstitute of Molecular Tumor Biology, University of Muenster, Muenster, Germany.
Tabea ErdmannDepartment of Medicine A, University Hospital Muenster, Muenster, Germany.
Georg LenzDepartment of Medicine A, University Hospital Muenster, Muenster, Germany.
Johannes RothInstitute of Immunology, University of Muenster, Muenster, Germany.
Thomas VoglInstitute of Immunology, University of Muenster, Muenster, Germany.
Marco PrinzInstitute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Martin DugasInstitute of Medical Informatics, University of Muenster, Muenster, Germany.
Ilse D JacobsenResearch Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knoell Institute, Jena, Germany.ORCID http://orcid.org/0000-0002-6033-9984
Frank RosenbauerInstitute of Molecular Tumor Biology, University of Muenster, Muenster, Germany. frank.rosenbauer@ukmuenster.de.ORCID http://orcid.org/0000-0001-7977-9421
Institute of Molecular Biology · DEUniversity Hospital Münster · DEUniversity of Freiburg · DEUniversity of Münster · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DERoche (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are essential first-line defense cells against invading pathogens, yet when inappropriately activated, their strong immune response can cause collateral tissue damage and contributes to immunological diseases. However, whether neutrophils can intrinsically titrate their immune response remains unknown. Here we conditionally deleted the Spi1 gene, which encodes the myeloid transcription factor PU.1, from neutrophils of mice undergoing fungal infection and then performed comprehensive epigenomic profiling. We found that as well as providing the transcriptional prerequisite for eradicating pathogens, the predominant function of PU.1 was to restrain the neutrophil defense by broadly inhibiting the accessibility of enhancers via the recruitment of histone deacetylase 1. Such epigenetic modifications impeded the immunostimulatory AP-1 transcription factor JUNB from entering chromatin and activating its targets. Thus, neutrophils rely on a PU.1-installed inhibitor program to safeguard their epigenome from undergoing uncontrolled activation, protecting the host against an exorbitant innate immune response.

Indexed as

AnimalsCandida albicansCandidiasisDisease ResistanceEpigenesis, GeneticEpigenomicsGene Expression ProfilingHumansMice, Inbred C57BLMice, KnockoutMice, TransgenicNeutrophilsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Survival AnalysisTrans-ActivatorsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID30911105
OpenAlexW2923207250

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.