Evidence map›Paper›PMID 36211444›Full record

ArticleFrontiers in immunology2022

Altered distribution and function of NK-cell subsets lead to impaired tumor surveillance in JAK2V617F myeloproliferative neoplasms.

Amanda Fernandes de Oliveira Costa, Leticia Olops Marani, Thiago Mantello Bianco, Adriana Queiroz Arantes, Izabela Aparecida Lopes, Diego Antonio Pereira-Martins, Leonardo Carvalho Palma, Priscila Santos Scheucher, Josiane Lilian Dos Santos Schiavinato, Larissa Sarri Binelli and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 49% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
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

16 authors at 5 institutions in 7 countries.

Amanda Fernandes de Oliveira CostaDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Leticia Olops MaraniDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Thiago Mantello BiancoDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Adriana Queiroz ArantesDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Izabela Aparecida LopesDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Diego Antonio Pereira-MartinsCenter for Cell-based Therapy, Regional Blood Center of Ribeirão Preto, Ribeirão Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.
Leonardo Carvalho PalmaDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Priscila Santos ScheucherDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Josiane Lilian Dos Santos SchiavinatoDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Larissa Sarri BinelliDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Cleide Araújo SilvaCenter for Cell-based Therapy, Regional Blood Center of Ribeirão Preto, Ribeirão Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.
Susumu S KobayashiDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
João Agostinho Machado-NetoDepartment of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Eduardo Magalhães RegoCenter for Cell-based Therapy, Regional Blood Center of Ribeirão Preto, Ribeirão Preto Medical School, University of São Paulo, Ribeirao Preto, Brazil.
Robert Samuel WelnerDivision Hematology/Oncology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
Lorena Lobo de Figueiredo-PontesDivision of Hematology, Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Universidade de São Paulo · BRClinics Hospital of Ribeirão Preto · BRBeth Israel Deaconess Medical Center · USNational Cancer Center Hospital East · JPUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cancer, tumor cells and their neoplastic microenvironment can sculpt the immunogenic phenotype of a developing tumor. In this context, natural killer (NK) cells are subtypes of lymphocytes of the innate immune system recognized for their potential to eliminate neoplastic cells, not only through direct cytolytic activity but also by favoring the development of an adaptive antitumor immune response. Even though the protective effect against leukemia due to NK-cell alloreactivity mediated by the absence of the KIR-ligand has already been shown, and some data on the role of NK cells in myeloproliferative neoplasms (MPN) has been explored, their mechanisms of immune escape have not been fully investigated. It is still unclear whether NK cells can affect the biology of BCR-ABL1-negative MPN and which mechanisms are involved in the control of leukemic stem cell expansion. Aiming to investigate the potential contribution of NK cells to the pathogenesis of MPN, we characterized the frequency, receptor expression, maturation profile, and function of NK cells from a conditional Jak2V617F murine transgenic model, which faithfully resembles the main clinical and laboratory characteristics of human polycythemia vera, and MPN patients. Immunophenotypic analysis was performed to characterize NK frequency, their subtypes, and receptor expression in both mutated and wild-type samples. We observed a higher frequency of total NK cells in JAK2V617F mutated MPN and a maturation arrest that resulted in low-numbered mature CD11b

Indexed as

Killer Cells, NaturalMyeloproliferative DisordersAnimalsHumansJanus Kinase 2LeukemiaLigandsMiceTumor MicroenvironmentJanus Kinase 2Ligandsflow cytometryJAK2v617F mutationmyeloproliferative neoplasmsnatural killer cellsnatural killer cells subsets

Identifiers

PMID36211444
PMCPMC9539129
OpenAlexW4296998035

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.