Evidence map›Paper›PMID 42051299›Full record

ArticlebioRxiv : the preprint server for biology2026

CXCR4 coordinates adhesion, migration, and development of human NK cells.

Shira E Eisman, Francesca Grossberg, Batya S Koenigsberg, David H McDermott, Frédérique van den Haak, Luis A Pedroza, Everardo Hegewisch-Solloa, Philip M Murphy, Emily M Mace

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Shira E EismanDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
Francesca GrossbergDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
Batya S KoenigsbergDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
David H McDermottLaboratory of Molecular Immunology, National Institute of Allergy and Infection Diseases, Bethesda MD USA.
Frédérique van den HaakDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
Luis A PedrozaDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
Everardo Hegewisch-SolloaDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.
Philip M MurphyLaboratory of Molecular Immunology, National Institute of Allergy and Infection Diseases, Bethesda MD USA.
Emily M MaceDepartment of Pediatrics, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York NY.ORCID 0000-0003-0226-7393

Funding

PREDOCTORAL TRAINING GRANT IN HUMAN GENETICS &DEVELOPMET32GM007088 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SHEN, MICHAEL M. · 1985 to 2020
$7.1M
DEFINING THE ROLE OF CELL MIGRATION IN HUMAN NK CELL DIFFERENTIATIONR01AI137073 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MACE, EMILY MARGARET · 2018 to 2022
$2.0M
NIAID NIH HHS R01 AI137073NIGMS NIH HHS T32 GM007088
6 · The paper itself

Abstract

Natural killer (NK) cells undergo stepwise differentiation from multipotent progenitors within secondary lymphoid tissues. Despite the central importance of the tissue microenvironment in their development, little is known about cell-cell interactions that regulate human NK cell trafficking and maturation. Here, we identify the chemokine receptor CXCR4 and its ligand CXCL12 as regulators of stromal-NK cell interactions required for NK cell maturation. We demonstrate that CXCR4 is expressed throughout human NK cell development in peripheral blood and tonsil, and CXCL12 is enriched in stromal niches containing developing NK cells. Pharmacologic blockade or genetic disruption of CXCR4 resulted in diminished adhesion to integrin ligands and high-resolution imaging demonstrated crosstalk between CXCR4 and integrins, providing a mechanistic basis for chemokine-dependent modulation of adhesion. Further, CXCR4 blockade resulted in altered contact-dependent motility on stromal cells and integrin ligands, with decreased stable stromal engagement and increased cell speed. Consistent with a requirement for these interactions, treatment with the CXCR4 antagonist plerixafor (AMD3100) impaired NK cell generation from CD34

Indexed as

cell migrationCXCR4NK cells

Identifiers

PMID42051299
PMCPMC13119322

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.