Evidence map›Paper›PMID 18390749›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Kruppel-like factor 4 is essential for inflammatory monocyte differentiation in vivo.

Jonathan K Alder, Robert W Georgantas, Richard L Hildreth, Ian M Kaplan, Sebastien Morisot, Xiaobing Yu, Michael McDevitt, Curt I Civin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

137 citing papers in PubMed, 209 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. KLF feedback loops in innate immunity.Frontiers in immunology · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Transcriptomic Profile of LinBMC genomics · 2024
    Article
  17. Review
  18. Transcription factor C/EBPα is required for the development of Ly6CProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Review
  20. Review

77 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

8 authors at 1 institution in 3 countries.

Jonathan K AlderDivisions of Immunology and Hematopoiesis, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
Robert W Georgantas
Richard L Hildreth
Ian M Kaplan
Sebastien Morisot
Xiaobing Yu
Michael McDevitt
Curt I Civin
Johns Hopkins University · US

Funding

THERAPEUTIC USE OF STEM CELLSP01CA070970 · NCI · JOHNS HOPKINS UNIVERSITY · PI CIVIN, CURT I · 1998 to 2012
$23.7M
NCI NIH HHS CA070970NCI NIH HHS P01 CA070970
6 · The paper itself

Abstract

Several members of the Kruppel-like factor (KLF) family of transcription factors play important roles in differentiation, survival, and trafficking of blood and immune cell types. We demonstrate in this study that hematopoietic cells from KLF4(-/-) fetal livers (FL) contained normal numbers of functional hematopoietic progenitor cells, were radioprotective, and performed as well as KLF4(+/+) cells in competitive repopulation assays. However, hematopoietic "KLF4(-/-) chimeras" generated by transplantation of KLF4(-/-) fetal livers cells into lethally irradiated wild-type mice completely lacked circulating inflammatory (CD115(+)Gr1(+)) monocytes, and had reduced numbers of resident (CD115(+)Gr1(-)) monocytes. Although the numbers and function of peritoneal macrophages were normal in KLF4(-/-) chimeras, bone marrow monocytic cells from KLF4(-/-) chimeras expressed lower levels of key trafficking molecules and were more apoptotic. Thus, our in vivo loss-of-function studies demonstrate that KLF4, previously shown to mediate proinflammatory signaling in human macrophages in vitro, is essential for differentiation of mouse inflammatory monocytes, and is involved in the differentiation of resident monocytes. In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. The inflammation-selective effects of loss-of-KLF4 and the gain-of-KLF4-induced monocytic differentiation in HL60 cells identify KLF4 as a key regulator of monocytic differentiation and a potential target for translational immune modulation.

Indexed as

AnimalsCarcinogensCell DifferentiationGranulocytesHematopoietic Stem CellsHL-60 CellsHumansInflammationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMacrophagesMiceMice, Inbred C57BLMice, KnockoutMonocytesMyelopoiesisCarcinogensKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsTetradecanoylphorbol Acetate

Identifiers

PMID18390749
PMCPMC3074963
OpenAlexW1533804294

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.