Evidence map›Paper›PMID 24874925›Full record

ArticlePloS one2014

KLF2--a negative regulator of pre-B cell clonal expansion and B cell activation.

Rebecca Winkelmann, Lena Sandrock, Jörg Kirberg, Hans-Martin Jäck, Wolfgang Schuh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Single-nuclei transcriptome analysis of IgMFrontiers in immunology · 2025
    Article
  4. Review
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  6. The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. A novel role for KLF14 in T regulatory cell differentiation.Cellular and molecular gastroenterology and hepatology · 2015
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Rebecca WinkelmannDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Lena SandrockDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Jörg KirbergDivision of Immunology, Paul-Ehrlich-Institut, Langen, Germany.
Hans-Martin JäckDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Wolfgang SchuhDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEPaul Ehrlich Institut · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maturation as well as antigen-dependent activation of B cells is accompanied by alternating phases of proliferation and quiescence. We and others have previously shown that Krüppel-like factor 2 (KLF2), a regulator of T cell quiescence and migration, is upregulated in small resting precursor (pre)-B cells after assembly of the immature pre-B cell receptor (pre-BCR) and is downregulated upon antigen-induced proliferation of mature B cells. These findings suggest that KLF2, besides its function in maintaining follicular B cell identity, peripheral B cell homeostasis and homing of antigen-specific plasma cells to the bone marrow, also controls clonal expansion phases in the B cell lineage. Here, we demonstrate that enforced expression of KLF2 in primary pre-B cells results in a severe block of pre-BCR-induced proliferation, upregulation of the cell cycle inhibitors p21 and p27 and downregulation of c-myc. Furthermore, retroviral KLF2 transduction of primary B cells impairs LPS-induced activation, favors apoptosis and results in reduced abundance of factors, such as AID, IRF4 and BLIMP1, that control the antigen-dependent phase of B cell activation and plasma cell differentiation. Hence, we conclude that KLF2 is not only a key player in terminating pre-B cell clonal expansion but also a potent suppressor of B cell activation.

Indexed as

AnimalsApoptosisB-LymphocytesClonal EvolutionCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Gene ExpressionGene Expression RegulationInterferon Regulatory Factor-4Interferon Regulatory FactorsKruppel-Like Transcription FactorsLymphocyte ActivationMiceMice, KnockoutPositive Regulatory Domain I-Binding Factor 1Precursor Cells, B-LymphoidCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Interferon Regulatory Factor-4Interferon Regulatory FactorsKlf2 protein, mouseKruppel-Like Transcription FactorsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseProto-Oncogene Proteins c-mycReceptors, Antigen, B-CellTranscription Factors

Identifiers

PMID24874925
PMCPMC4038547
OpenAlexW2036077632

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.