Evidence map›Paper›PMID 40437214›Full record

ArticleCommunications medicine2025

Natural killer cells adopt an activated and decidual-like phenotype after autologous hematopoietic stem cell transplantation in children with cancer.

Gabirel Astarloa-Pando, Diego Polanco-Alonso, Víctor Sandá, Ane Orrantia, Ainhoa Amarilla-Irusta, Silvia Pérez-Fernández, Raquel Pérez-Garay, Arrate Sevilla, Ainara Lopez-Pardo, Aritz Tijero and 9 more

Abstract read
In one paragraph

Article in Communications medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

19 authors.

Gabirel Astarloa-PandoImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Diego Polanco-AlonsoImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID http://orcid.org/0000-0002-4017-5185
Víctor SandáImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Ane OrrantiaImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Ainhoa Amarilla-IrustaImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Silvia Pérez-FernándezBioinformatics, Biostatistics and Information Systems Platform, Biobizkaia Health Research Institute, Barakaldo, Spain.
Raquel Pérez-GarayImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Arrate SevillaImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Ainara Lopez-PardoImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID http://orcid.org/0000-0001-6637-4396
Aritz TijeroImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
José J ÚrizBiogipuzkoa Health Research Institute, Service of Pediatrics, Donostia University Hospital, Donostia-San Sebastián, Spain.
Mercedes ReyBiogipuzkoa Health Research Institute, Service of Immunology, Donostia University Hospital, Donostia-San Sebastián, Spain.
Itziar AstigarragaPediatric Oncology Group, Department of Pediatrics, Biobizkaia Health Research Institute, Cruces University Hospital, Barakaldo, Spain.
Bárbara Manzanares-MartinMaimónides Biomedical Research Institute of Córdoba (IMIBIC), Immunology and Allergy Department of Reina Sofía University Hospital and Transfusion, Tissue and Cells Centre (CTTC), Córdoba, Spain.
Aitor Zarandona-GaraiBioinformatics, Biostatistics and Information Systems Platform, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID http://orcid.org/0009-0001-9815-2779
Naiara G BediagaBioinformatics, Biostatistics and Information Systems Platform, Biobizkaia Health Research Institute, Barakaldo, Spain.
Laura AmoImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Olatz ZenarruzabeitiaImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain.
Francisco BorregoImmunopathology Group, Biobizkaia Health Research Institute, Barakaldo, Spain. francisco.borregorabasco@bio-bizkaia.eus.ORCID http://orcid.org/0000-0002-3105-981X

Funding

Consejería de Salud, Junta de Andalucía (Ministry of Health, Andalusian Regional Government) RH-0060-2020Fundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PPLAB212164POLAFundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PPLAB223829TIJEFundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PRDVZ21440ASTAFundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PRDVZ234209AMARFundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PROYE16074BORRIkerbasque, Basque Foundation for Science COFUND program H2020-MSCA-COFUND-2020-101034228-WOLFRAM2Osasun Saila, Eusko Jaurlaritzako (Departamento de Salud, Gobierno Vasco) BIO20/CI/009
6 · The paper itself

Abstract

backgroundNatural killer (NK) cells are among the first immune cell populations to recover after autologous hematopoietic stem cell transplantation (autoHSCT ), yet their dynamic function in pediatric patients remains understudied. Investigating NK cell recovery could improve understanding of post-autoHSCT immune reconstitution and optimize clinical outcomes.

methodsWe characterized NK cells in 13 children (male: 8; female: 5; age range: 3-11 years) with various tumors before and up to 6 months after autoHSCT. Multiparametric flow cytometry analyses and plasma cytokine level determinations were performed. In vitro experiments, including single-cell RNA sequencing, were conducted to elucidate post-autoHSCT changes in the NK cell repertoire using 8 adult healthy donors (male: 5; female: 3; age range: 25-62 years).

resultsKey findings highlight a transient decidual-like NK cell phenotype emerging early post-transplant. These cells are immature and activated, with increased inhibitory receptor expression and diminished activating receptor levels. This activated and decidual-like phenotype is characterized by elevated expression of CD56, CD9, CD49a, CD151, CD38, HLA-DR, and CD55. Plasma levels of several cytokines are associated with the observed changes in NK cells' phenotype. In addition, in vitro experiments recapitulate the alterations observed in NK cells shortly after autoHSCT. Specifically, results demonstrate that the combination of IL-15 and TGF-β induces this distinctive phenotype on NK cells after autoHSCT. Finally, we observe a positive correlation between relapse and the percentage of CD56

conclusionsAltogether, our findings provide valuable insights into the physiopathology of NK cells during immune system reconstitution after autoHSCT and can potentially help in the management of cancer in children.

Identifiers

PMID40437214
PMCPMC12120011

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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.