Evidence map›Paper›PMID 25138665›Full record

ArticleMucosal immunology2015

An in vitro model of innate lymphoid cell function and differentiation.

D S J Allan, C L Kirkham, O A Aguilar, L C Qu, P Chen, J H Fine, P Serra, G Awong, J L Gommerman, J C Zúñiga-Pflücker and 1 more

Open access · bronzeAbstract read
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In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

56 citing papers in PubMed, 74 citations in OpenAlex.

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  19. Review
  20. GPX4 restricts ferroptosis of NKp46Cell death & disease · 2024
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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

11 authors at 2 institutions in 1 country.

D S J Allan1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
C L Kirkham1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
O A Aguilar1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
L C Qu1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
P Chen1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
J H Fine1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
P Serra1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
G Awong1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
J L GommermanDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada.
J C Zúñiga-Pflücker1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
J R Carlyle1] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [2] Sunnybrook Research Institute, Toronto, Ontario, Canada.
Sunnybrook Health Science Centre · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Innate lymphoid cells (ILC) are RAG-independent lymphocytes with important roles in innate immunity, and include group-1 (natural killer (NK) cell, ILC1), group-2 (ILC2), and group-3 (lymphoid tissue inducer (LTi), NCR(+) ILC3) subsets. Group-3 ILC express Rorγt, produce interleukin (IL)-22, and are critically important in the normal function of mucosal tissues. Here, we describe a novel model cell line for the study of ILC function and differentiation. The parental MNK cell line, derived from NKR-P1B(+) fetal thymocytes, shows a capacity to differentiate in γc cytokines. One IL-7-responsive subline, designated MNK-3, expresses Rorγt and produces high levels of IL-22 in response to IL-23 and IL-1β stimulation. MNK-3 cells display surface markers and transcript expression characteristic of group-3 ILC, including IL-7Rα (CD127), c-kit (CD117), CCR6, Thy1 (CD90), RANK, RANKL, and lymphotoxin (LTα1β2). Using an in vitro assay of LTi cell activity, MNK-3 cells induce ICAM-1 and VCAM-1 expression on stromal cells in a manner dependent upon LTα1β2 expression. A second IL-2-responsive subline, MNK-1, expresses several NK cell receptors, perforin and granzymes, and shows some cytotoxic activity. Thus, MNK-1 cells serve as a model of ILC1/NK development and differentiation, whereas MNK-3 cells provide an attractive in vitro system to study the function of ILC3/LTi cells.

Indexed as

Immunity, InnateAnimalsAntigens, SurfaceCell DifferentiationCell LineageCluster AnalysisCytokinesGene Expression ProfilingGene Expression RegulationImmunophenotypingLymphocytesLymphocyte SubsetsMiceNuclear Receptor Subfamily 1, Group F, Member 3PhenotypeReceptors, Natural Killer CellAntigens, SurfaceCytokinesNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Natural Killer Cell

Identifiers

PMID25138665
OpenAlexW1973113100

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.