Evidence map›Paper›PMID 33593878›Full record

ArticleLife science alliance2021

Short-term IL-15 priming leaves a long-lasting signalling imprint in mouse NK cells independently of a metabolic switch.

Thuy T Luu, Laurent Schmied, Ngoc-Anh Nguyen, Clotilde Wiel, Stephan Meinke, Dara K Mohammad, Martin Bergö, Evren Alici, Nadir Kadri, Sridharan Ganesan and 1 more

Abstract read
In one paragraph

Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. piggyBac system to co-express NKG2D CAR and IL-15 to augment theMolecular therapy. Methods & clinical development · 2021
    Article
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.

Thuy T LuuDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-2619-1357
Laurent SchmiedDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-3303-881X
Ngoc-Anh NguyenDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0003-3367-8048
Clotilde WielDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Stephan MeinkeDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0003-4489-9727
Dara K MohammadDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0001-9201-0991
Martin BergöDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-6915-7140
Evren AliciDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.
Nadir KadriDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.
Sridharan GanesanDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-6783-0100
Petter HöglundDepartment of Medicine Huddinge, Centre for Haematology and Regenerative Medicine (HERM), Karolinska Institutet, Huddinge, Sweden petter.hoglund@ki.se.ORCID 0000-0002-9233-626X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-15 priming of NK cells is a broadly accepted concept, but the dynamics and underlying molecular mechanisms remain poorly understood. We show that as little as 5 min of IL-15 treatment in vitro, followed by removal of excess cytokines, results in a long-lasting, but reversible, augmentation of NK cell responsiveness upon activating receptor cross-linking. In contrast to long-term stimulation, improved NK cell function after short-term IL-15 priming was not associated with enhanced metabolism but was based on the increased steady-state phosphorylation level of signalling molecules downstream of activating receptors. Inhibition of JAK3 eliminated this priming effect, suggesting a cross talk between the IL-15 receptor and ITAM-dependent activating receptors. Increased signalling molecule phosphorylation levels, calcium flux, and IFN-γ secretion lasted for up to 3 h after IL-15 stimulation before returning to baseline. We conclude that IL-15 rapidly and reversibly primes NK cell function by modulating activating receptor signalling. Our findings suggest a mechanism by which NK cell reactivity can potentially be maintained in vivo based on only brief encounters with IL-15 trans-presenting cells.

Indexed as

Energy MetabolismSignal TransductionAnimalsBiomarkersCytokinesImmunophenotypingInterferon-gammaInterleukin-15Interleukin-2Killer Cells, NaturalLymphocyte ActivationMicePhosphorylationReactive Oxygen SpeciesBiomarkersCytokinesInterferon-gammaInterleukin-15Interleukin-2Reactive Oxygen Species

Identifiers

PMID33593878
PMCPMC7918643

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.