Evidence map›Paper›PMID 35813574›Full record

ArticleOncoimmunology2022

PD-1 is expressed in cytotoxic granules of NK cells and rapidly mobilized to the cell membrane following recognition of tumor cells.

Cecilia Pesini, Sandra Hidalgo, Maykel A Arias, Llipsy Santiago, Carlota Calvo, Maitane Ocariz-Díez, Dolores Isla, Pilar M Lanuza, M José Agustín, Eva M Galvez and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2022. 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
1.2field-weighted citation impact, top 22% 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, 14 citations in OpenAlex.

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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

12 authors at 5 institutions in 1 country.

Cecilia PesiniImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0002-8707-2722
Sandra HidalgoImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.
Maykel A AriasImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0002-9730-2210
Llipsy SantiagoImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0002-1861-5981
Carlota CalvoImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.
Maitane Ocariz-DíezMedical Oncology Department, Aragón Health Research Institute (IIS Aragón), Hospital Clinico Universitario Lozano Blesa, Zaragoza, Spain.
Dolores IslaMedical Oncology Department, Aragón Health Research Institute (IIS Aragón), Hospital Clinico Universitario Lozano Blesa, Zaragoza, Spain.
Pilar M LanuzaImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0001-7328-2094
M José AgustínPharmacy Department, Hospital Universitario Miguel Servet, Zaragoza, Spain.
Eva M GalvezCSIC, Instituto de Carboquimica (ICB), Zaragoza, Spain.
Ariel Ramírez-LabradaImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0002-3888-7036
Julián PardoImmunotherapy, Inflammation and Cancer, Aragón Health Research Institute (IIS Aragón), Biomedical Research Centre of Aragón (CIBA), Zaragoza, Spain.ORCID 0000-0003-0154-0730
Universidad de Zaragoza · ESInstituto de Investigación Sanitaria Aragón · ESHospital Clínico Universitario Lozano Blesa · ESHospital Universitario Miguel Servet · ESInstituto de Carboquímica · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of the T cell-related inhibitory checkpoint PD-1 to the regulation of NK cell activity is still not clear with contradictory results concerning its expression and role in the modulation of NK cell cytotoxicity. We provide novel key findings on the mechanism involved in the regulation of PD-1 expression on NK cell membrane and its functional consequences for the elimination of cancer cells. In contrast to freshly isolated NK cells from cancer patients, those from healthy donors did not express PD-1 on the cell membrane. However, when healthy NK cells were incubated with tumor target cells, membrane PD-1 expression increased, concurrent with the CD107a surface mobilization. This finding suggested that PD-1 was translocated to the cell membrane during NK cell degranulation after contact with target cells. Indeed, cytosolic PD-1 was expressed in freshly-isolated-NK cells and partly co-localized with CD107a and GzmB, confirming that membrane PD-1 corresponded to a pool of preformed PD-1. Moreover, NK cells that had mobilized PD-1 to the cell membrane presented a significantly reduced anti-tumor activity on PD-L1-expressing-tumor cells

Indexed as

Antineoplastic AgentsNeoplasmsCell MembraneHumansImmunotherapyKiller Cells, NaturalLymphocyte ActivationAntineoplastic Agentsadoptive cell therapycell cytotoxicitynatural killer cellsPD-1

Identifiers

PMID35813574
PMCPMC9262365
OpenAlexW4284889299

What OpenQuestion holds

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LicenceCC BY-NC
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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.