Evidence map›Paper›PMID 29907883›Full record

ArticleCellular & molecular immunology2019

B cell development is critically dependent on NFATc1 activity.

Sabrina Giampaolo, Gabriela Wójcik, Stefan Klein-Hessling, Edgar Serfling, Amiya K Patra

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. A comprehensive full-length transcriptome atlas across multiple organs of an Indian yak breed-Arunachali.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  2. Antioxidants (Basel, Switzerland) · 2026
    Review
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  6. FcRL1, a New B-Cell-Activating Co-Receptor.International journal of molecular sciences · 2025
    Review
  7. Article
  8. A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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 2 countries.

Sabrina GiampaoloDepartment of Molecular Pathology, Institute of Pathology, University of Würzburg, Josef Schneider-Str. 2, 97080, Würzburg, Germany.
Gabriela WójcikInstitute of Translational and Stratified Medicine, Faculty of Medicine and Dentistry, University of Plymouth, Plymouth, PL6 8BU, UK.
Stefan Klein-HesslingDepartment of Molecular Pathology, Institute of Pathology, University of Würzburg, Josef Schneider-Str. 2, 97080, Würzburg, Germany.
Edgar SerflingDepartment of Molecular Pathology, Institute of Pathology, University of Würzburg, Josef Schneider-Str. 2, 97080, Würzburg, Germany.
Amiya K PatraInstitute of Translational and Stratified Medicine, Faculty of Medicine and Dentistry, University of Plymouth, Plymouth, PL6 8BU, UK. amiya.patra@plymouth.ac.uk.
University of Würzburg · DEUniversity of Plymouth · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B cell development in bone marrow is a precisely regulated complex process. Through successive stages of differentiation, which are regulated by a multitude of signaling pathways and an array of lineage-specific transcription factors, the common lymphoid progenitors ultimately give rise to mature B cells. Similar to early thymocyte development in the thymus, early B cell development in bone marrow is critically dependent on IL-7 signaling. During this IL-7-dependent stage of differentiation, several transcription factors, such as E2A, EBF1, and Pax5, among others, play indispensable roles in B lineage specification and maintenance. Although recent studies have implicated several other transcription factors in B cell development, the role of NFATc1 in early B cell developmental stages is not known. Here, using multiple gene-manipulated mouse models and applying various experimental methods, we show that NFATc1 activity is vital for early B cell differentiation. Lack of NFATc1 activity in pro-B cells suppresses EBF1 expression, impairs immunoglobulin gene rearrangement, and thereby preBCR formation, resulting in defective B cell development. Overall, deficiency in NFATc1 activity arrested the pro-B cell transition to the pre-B cell stage, leading to severe B cell lymphopenia. Our findings suggest that, along with other transcription factors, NFATc1 is a critical component of the signaling mechanism that facilitates early B cell differentiation.

Indexed as

AnimalsB-LymphocytesBone Marrow CellsCell DifferentiationCell LineageCells, CulturedInterleukin-7Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutNFATC Transcription FactorsPrecursor Cells, B-LymphoidSignal TransductionTrans-ActivatorsEbf1 protein, mouseInterleukin-7Nfatc1 protein, mouseNFATC Transcription FactorsTrans-ActivatorsDifferentiationEBF1NFATc1Pre-BPro-B

Identifiers

PMID29907883
PMCPMC6474210
OpenAlexW2808538698

What OpenQuestion holds

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LicenceCC BY
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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.