Evidence map›Paper›PMID 24086722›Full record

ArticlePloS one2013

Interleukin 15 primes natural killer cells to kill via NKG2D and cPLA2 and this pathway is active in psoriatic arthritis.

Fangming Tang, Benjamin Sally, Cezary Ciszewski, Valerie Abadie, Shane A Curran, Veronika Groh, Oliver Fitzgerald, Robert J Winchester, Bana Jabri

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Deciphering the Complex Immunopathogenesis of Alopecia Areata.International journal of molecular sciences · 2024
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  9. Human intraepithelial lymphocytes.Mucosal immunology · 2018
    Review
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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

9 authors at 4 institutions in 2 countries.

Fangming TangDepartment of Medicine, University of Chicago, Chicago, Illinois, United States of America.
Benjamin Sally
Cezary Ciszewski
Valerie Abadie
Shane A Curran
Veronika Groh
Oliver Fitzgerald
Robert J Winchester
Bana Jabri
University of Chicago · USColumbia University · USFred Hutch Cancer Center · USSt. Vincent's University Hospital · IE

Funding

Innate and adaptive immunity in celiac diseaseR01DK067180 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2005 to 2024
$8.5M
Regulation of normal human IEL by NKG2D and IL-15R01DK058727 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2001 to 2010
$2.7M
NIDDK NIH HHS R01 DK058727NIDDK NIH HHS R01 DK067180
6 · The paper itself

Abstract

NK cells are large granular lymphocytes that form a critical component of the innate immune system, whose functions include the killing of cells expressing stress-induced molecules. It is increasingly accepted that despite being considered prototypical effector cells, NK cells require signals to reach their full cytotoxic potential. We previously showed that IL-15 is capable of arming CD8 effector T cells to kill independently of their TCR via NKG2D in a cPLA2-dependent process. As NK cells also express NKG2D, we wanted to investigate whether this pathway functioned in an analogous manner and if resting NK cells could be primed to the effector phase by IL-15. Furthermore, to establish relevance to human disease we studied a possible role for this pathway in the pathogenesis of psoriatic arthritis, since there are aspects of this disease that suggest a potential effector role for the innate immune system. We found that PsA patients had upregulated IL-15 and MIC in their affected synovial tissues, and that this unique inflammatory environment enabled NK cell activation and killing via NKG2D and cPLA2. Moreover, we were able to reproduce the phenotype of joint NK cells from blood NK cells by incubating them with IL-15. Altogether, these findings suggest a destructive role for NK cells when activated by environmental stress signals during the pathogenesis of PsA and demonstrate that IL-15 is capable of priming resting NK cells in tissues to the effector phase.

Indexed as

Arthritis, PsoriaticCytokinesFlow CytometryGene Expression RegulationHumansImmunohistochemistryInterleukin-15Killer Cells, NaturalNK Cell Lectin-Like Receptor Subfamily KPhospholipases A2, CytosolicRNA, Small InterferingSignal TransductionTransfectionCytokinesInterleukin-15KLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KPhospholipases A2, CytosolicRNA, Small Interfering

Identifiers

PMID24086722
PMCPMC3783406
OpenAlexW2011723704

What OpenQuestion holds

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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.