Evidence map›Paper›PMID 25403444›Full record

ArticleThe Journal of experimental medicine2014

CXCR4 and a cell-extrinsic mechanism control immature B lymphocyte egress from bone marrow.

Thomas C Beck, Ana Cordeiro Gomes, Jason G Cyster, João P Pereira

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  8. Review
  9. Review
  10. Revisiting MSC heterogeneity: significance of the CD73Frontiers in bioengineering and biotechnology · 2026
    Article
  11. Lymphotoxin beta receptorInfection and immunity · 2025
    Article
  12. Article
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  14. Review
  15. Review
  16. Article
  17. Article
  18. Tenascin-C regulates CXCR4Frontiers in immunology · 2025
    Article
  19. Review
  20. Article

38 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

4 authors at 2 institutions in 1 country.

Thomas C BeckDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Ana Cordeiro GomesDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520.
Jason G CysterHoward Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143 Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
João P PereiraDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 joao.pereira@yale.edu.
Yale University · USHoward Hughes Medical Institute · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
Cellular and molecular analysis of B lymphocyte development and selectionR01AI113040 · NIAID · YALE UNIVERSITY · PI JOAO PEREIRA · 2014 to 2026
$6.0M
Control of B-lineage cell migration during differentiation in bone marrowR56AI098996 · NIAID · YALE UNIVERSITY · PI PEREIRA, JOAO · 2012 to 2012
$415k
Howard Hughes Medical InstituteNCI NIH HHS P30 CA016359NIAID NIH HHS R01 AI113040NIAID NIH HHS R01AI113040NIAID NIH HHS R56 AI098996NIAID NIH HHS R56AI098996
6 · The paper itself

Abstract

Leukocyte residence in lymphoid organs is controlled by a balance between retention and egress-promoting chemoattractants sensed by pertussis toxin (PTX)-sensitive Gαi protein-coupled receptors (GPCRs). Here, we use two-photon intravital microscopy to show that immature B cell retention within bone marrow (BM) was strictly dependent on amoeboid motility mediated by CXCR4 and CXCL12 and by α4β1 integrin-mediated adhesion to VCAM-1. However, B lineage cell egress from BM is independent of PTX-sensitive GPCR signaling. B lineage cells expressing PTX rapidly exited BM even though their motility within BM parenchyma was significantly reduced. Our experiments reveal that when immature B cells are near BM sinusoids their motility is reduced, their morphology is predominantly rounded, and cells reverse transmigrate across sinusoidal endothelium in a largely nonamoeboid manner. Immature B cell egress from BM was dependent on a twofold CXCR4 down-regulation that was antagonized by antigen-induced BCR signaling. This passive mode of cell egress from BM also contributes significantly to the export of other hematopoietic cells, including granulocytes, monocytes, and NK cells, and is reminiscent of erythrocyte egress.

Indexed as

AnimalsB-LymphocytesBone Marrow CellsCell DifferentiationCell LineageCell MovementCell ShapeDown-RegulationIntegrin alpha4beta1Mice, Inbred C57BLReceptors, Antigen, B-CellReceptors, CXCR4Signal TransductionVascular Cell Adhesion Molecule-1CXCR4 protein, mouseIntegrin alpha4beta1Receptors, Antigen, B-CellReceptors, CXCR4Vascular Cell Adhesion Molecule-1

Identifiers

PMID25403444
PMCPMC4267240
OpenAlexW2137536511

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.