Evidence map›Paper›PMID 29296921›Full record

ArticleBlood advances2017

Interleukins 12 and 15 induce cytotoxicity and early NK-cell differentiation in type 3 innate lymphoid cells.

Ana Raykova, Paolo Carrega, Frank M Lehmann, Robert Ivanek, Vanessa Landtwing, Isaak Quast, Jan D Lünemann, Daniela Finke, Guido Ferlazzo, Obinna Chijioke and 1 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  11. Innate lymphoid cells and cancer.Nature immunology · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. The Metabolic Basis of ILC Plasticity.Frontiers in immunology · 2022
    Review
  18. Plasticity of Innate Lymphoid Cells in Cancer.Frontiers in immunology · 2022
    Review
  19. Article
  20. 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

11 authors at 6 institutions in 3 countries.

Ana RaykovaViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Paolo CarregaLaboratory of Immunology and Biotherapy, Department of Human Pathology, University of Messina, Messina, Italy.
Frank M LehmannUniversity Children's Hospital of Basel, Basel, Switzerland.
Robert IvanekBioinformatics Core Facility, Department of Biomedicine, University Hospital Basel/University of Basel, Basel, Switzerland.
Vanessa LandtwingViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Isaak QuastDepartment of Immunology and Pathology, Monash University, Melbourne, VIC, Australia.
Jan D LünemannNeuroinflammation, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Daniela FinkeUniversity Children's Hospital of Basel, Basel, Switzerland.
Guido FerlazzoLaboratory of Immunology and Biotherapy, Department of Human Pathology, University of Messina, Messina, Italy.
Obinna ChijiokeViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Christian MünzViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
University of Zurich · CHUniversity Children’s Hospital Basel · CHAzienda Ospedaliera Universitaria Policlinico "G. Martino" · ITMonash University · AUUniversity of Basel · CHUniversity of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 3 innate lymphoid cells (ILC3s) fulfill protective functions at mucosal surfaces via cytokine production. Although their plasticity to become ILC1s, the innate counterparts of type 1 helper T cells, has been described previously, we report that they can differentiate into cytotoxic lymphocytes with many characteristics of early differentiated natural killer (NK) cells. This transition is promoted by the proinflammatory cytokines interleukin 12 (IL-12) and IL-15, and correlates with expression of the master transcription factor of cytotoxicity, eomesodermin (Eomes). As revealed by transcriptome analysis and flow cytometric profiling, differentiated ILC3s express CD94, NKG2A, NKG2C, CD56, and CD16 among other NK-cell receptors, and possess all components of the cytotoxic machinery. These characteristics allow them to recognize and kill leukemic cells with perforin and granzymes. Therefore, ILC3s can be harnessed for cytotoxic responses via differentiation under the influence of proinflammatory cytokines.

Identifiers

PMID29296921
PMCPMC5745129
OpenAlexW2773038084

What OpenQuestion holds

Textmetadata
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.