Evidence map›Paper›PMID 30538245›Full record

ArticleNature communications2018

CSF1R regulates the dendritic cell pool size in adult mice via embryo-derived tissue-resident macrophages.

Gulce Itir Percin, Jiri Eitler, Andrea Kranz, Jun Fu, Jeffrey W Pollard, Ronald Naumann, Claudia Waskow

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting TREM2Cancer communications (London, England) · 2026
    Article
  4. Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  15. CSF-1 maintains pathogenic but not homeostatic myeloid cells in the central nervous system during autoimmune neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

7 authors at 4 institutions in 2 countries.

Gulce Itir PercinRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Fetscherstr. 74, 01307, Dresden, Germany.
Jiri EitlerRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Fetscherstr. 74, 01307, Dresden, Germany.
Andrea KranzGenomics, Biotechnology Center, TU Dresden, BioInnovationsZentrum, Tatzberg 47-49, 01307, Dresden, Germany.ORCID http://orcid.org/0000-0002-7481-0220
Jun FuGenomics, Biotechnology Center, TU Dresden, BioInnovationsZentrum, Tatzberg 47-49, 01307, Dresden, Germany.
Jeffrey W PollardMRC and University of Edinburgh Centre for Reproductive Health, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.ORCID http://orcid.org/0000-0003-4579-0053
Ronald NaumannMax Planck Institute of Molecular Cell Biology and Genetics, Transgenic Core Facility, Pfotenhauerstr. 108, 01307, Dresden, Germany.
Claudia WaskowRegeneration in Hematopoiesis and Animal Models in Hematopoiesis, Institute for Immunology, Fetscherstr. 74, 01307, Dresden, Germany. Claudia.Waskow@leibniz-fli.de.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DETechnische Universität Dresden · DEEdinburgh Cancer Research · GBMax Planck Institute of Molecular Cell Biology and Genetics · DE

Funding

Medical Research Council G1002033Medical Research Council MR/K015710/1Medical Research Council MR/N022556/1Wellcome Trust
6 · The paper itself

Abstract

Regulatory mechanisms controlling the pool size of spleen dendritic cells (DC) remain incompletely understood. DCs are continuously replenished from hematopoietic stem cells, and FLT3-mediated signals cell-intrinsically regulate homeostatic expansion of spleen DCs. Here we show that combining FLT3 and CSF1R-deficiencies results in specific and complete abrogation of spleen DCs in vivo. Spatiotemporally controlled CSF1R depletion reveals a cell-extrinsic and non-hematopoietic mechanism for DC pool size regulation. Lack of CSF1R-mediated signals impedes the differentiation of spleen macrophages of embryonic origin, and the resulted macrophage depletion during development or in adult mice results in loss of DCs. Moreover, embryo-derived macrophages are important for the physiologic regeneration of DC after activation-induced depletion in situ. In summary, we show that the differentiation of DC and their regeneration relies on ontogenetically distinct spleen macrophages, thereby providing a novel regulatory principle that may also be important for the differentiation of other hematopoietic cell types.

Indexed as

AnimalsCell DifferentiationDendritic CellsFemalefms-Like Tyrosine Kinase 3MacrophagesMaleMiceMice, KnockoutReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSpleenCsf1r protein, mouseFlt3 protein, mousefms-Like Tyrosine Kinase 3Receptors, Granulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID30538245
PMCPMC6290072
OpenAlexW2902377348

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.