Evidence map›Paper›PMID 24810486›Full record

ArticleEuropean journal of immunology2014

Dendritic cell development requires histone deacetylase activity.

Heike Chauvistré, Caroline Küstermann, Nina Rehage, Theresa Klisch, Saskia Mitzka, Piritta Felker, Stefan Rose-John, Martin Zenke, Kristin M Seré

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. ACY-1215 ameliorates experimental colitis by inhibiting dendritic cell maturation and Th1/Th17 responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
  3. Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
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  17. Article
  18. Examination of the role of sphingosine kinase 2 in a murine model of systemic lupus erythematosus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  19. Article
  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 2 institutions in 1 country.

Heike ChauvistréInstitute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany.
Caroline Küstermann
Nina Rehage
Theresa Klisch
Saskia Mitzka
Piritta Felker
Stefan Rose-John
Martin Zenke
Kristin M Seré
RWTH Aachen University · DEKiel University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DCs develop from multipotent progenitors (MPPs), which commit into DC-restricted common dendritic cell progenitors (CDPs). CDPs further differentiate into classical DCs (cDCs) and plasmacytoid DCs (pDCs). Here, we studied the impact of histone acetylation on DC development in C57BL/6 mice by interfering with histone acetylation and deacetylation, employing histone deacetylase (HDAC) inhibitors. We observed that commitment of MPPs into CDPs was attenuated by HDAC inhibition and that pDC development was specifically blocked. Gene expression profiling revealed that HDAC inhibition prevents establishment of a DC-specific gene expression repertoire. Importantly, protein levels of the core DC transcription factor PU.1 were reduced in HDAC inhibitor-treated cells and consequently PU.1 recruitment at PU.1 target genes Fms-like tyrosine kinase 3 (Flt3), interferon regulatory factor 8 (IRF8), and PU.1 itself was impaired. Thus, our results demonstrate that attenuation of PU.1 expression by HDAC inhibition causes reduced expression of key DC regulators, which results in attenuation of DC development. We propose that chromatin modifiers, such as HDACs, are required for establishing a DC gene network, where Flt3/STAT3 signaling drives PU.1 and IRF8 expression and DC development. Taken together, our study identifies HDACs as critical regulators of DC lineage commitment and development.

Indexed as

AcetylationAnimalsCell DifferentiationCells, CulturedChromatinDendritic Cellsfms-Like Tyrosine Kinase 3Gene ExpressionGene Expression ProfilingHistone DeacetylasesInterferon Regulatory Factor-8Interferon Regulatory FactorsMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDChromatinFlt3 protein, mousefms-Like Tyrosine Kinase 3Histone DeacetylasesInterferon Regulatory Factor-8Interferon Regulatory FactorsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Stat3 protein, mouseSTAT3 Transcription FactorTrans-ActivatorsDendritic cellsFlt3HDACHistone acetylationPU.1

Identifiers

PMID24810486
PMCPMC4209797
OpenAlexW1545656771

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.