Evidence map›Paper›PMID 38118422›Full record

ArticleCell reports. Medicine2023

FLT3L-dependent dendritic cells control tumor immunity by modulating Treg and NK cell homeostasis.

Paul Régnier, Mathias Vetillard, Adèle Bansard, Eméranne Pierre, Xinyue Li, Nicolas Cagnard, Emmanuel L Gautier, Pierre Guermonprez, Bénédicte Manoury, Katrina Podsypanina and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-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

18 citing papers in PubMed, 17 citations in OpenAlex.

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  11. Microbiology spectrum · 2025
    Article
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  15. Microwave Ablation Combined with Flt3L Provokes Tumor-Specific Memory CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Paul RégnierInstitut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Sorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department of Internal Medicine and Clinical Immunology, DMU3ID, Paris, France.
Mathias VetillardUniversité de Paris Cité, Centre for Inflammation Research, INSERM U1149, CNRS ERL8252, Paris, France; Dendritic Cells and Adaptive Immunity Unit, Institut Pasteur, Paris, France.
Adèle BansardInstitut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Université Paris Cité, Faculté de Médecine, Paris, France.
Eméranne PierreUniversité Paris Cité, Faculté de Médecine, Paris, France.
Xinyue LiSorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France.
Nicolas CagnardStructure Fédérative de Recherche Necker, Université Paris Descartes, Paris, France.
Emmanuel L GautierInserm, UMR_S1166, Sorbonne Université, Hôpital Pitié-Salpêtrière, Paris, France.
Pierre GuermonprezUniversité de Paris Cité, Centre for Inflammation Research, INSERM U1149, CNRS ERL8252, Paris, France; Dendritic Cells and Adaptive Immunity Unit, Institut Pasteur, Paris, France.
Bénédicte ManouryInstitut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France.
Katrina PodsypaninaInstitut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Institut Curie, PSL Research University, CNRS, Sorbonne Université, UMR3664, Paris, France.
Guillaume Darrasse-JèzeInstitut Necker Enfants Malades, INSERM U1151, CNRS UMR-8253, Université Paris Cité, Paris, France; Sorbonne Université, INSERM, UMR_S959, Immunology-Immunopathology-Immunotherapy, Paris, France; Université Paris Cité, Faculté de Médecine, Paris, France. Electronic address: guillaume.darrasse-jeze@inserm.fr.
Centre National de la Recherche Scientifique · FRDélégation Paris 5 · FRInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FLT3-L-dependent classical dendritic cells (cDCs) recruit anti-tumor and tumor-protecting lymphocytes. We evaluate cancer growth in mice with low, normal, or high levels of cDCs. Paradoxically, both low or high numbers of cDCs improve survival in mice with melanoma. In low cDC context, tumors are restrained by the adaptive immune system through influx of effector T cells and depletion of Tregs and NK cells. High cDC numbers favor the innate anti-tumor response, with massive recruitment of activated NK cells, despite high Treg infiltration. Anti CTLA-4 but not anti PD-1 therapy synergizes with FLT3-L therapy in the cDC

Indexed as

NeoplasmsT-Lymphocytes, RegulatoryAnimalsDendritic CellsHomeostasisHumansKiller Cells, NaturalMiceCTLA-4dendritic cellseffector T cellsFlt3-LFoxp3(+) regulatory T cellsnatural killer cellsPD-1TARGETTCGAtranscriptometumor microenvironmentZbtb46

Identifiers

PMID38118422
PMCPMC10772324
OpenAlexW4389955978

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.