Evidence map›Paper›PMID 37486946›Full record

ArticlePLoS pathogens2023

Streptococcus pneumoniae drives specific and lasting Natural Killer cell memory.

Tiphaine M N Camarasa, Júlia Torné, Christine Chevalier, Orhan Rasid, Melanie A Hamon

Abstract read
In one paragraph

Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Leukocyte kinetics and bacterial clearance duringAmerican journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  8. 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

5 authors.

Tiphaine M N CamarasaChromatin and Infection Unit, Institut Pasteur, Paris, France.
Júlia TornéChromatin and Infection Unit, Institut Pasteur, Paris, France.
Christine ChevalierChromatin and Infection Unit, Institut Pasteur, Paris, France.
Orhan RasidChromatin and Infection Unit, Institut Pasteur, Paris, France.ORCID 0000-0002-7040-9587
Melanie A HamonChromatin and Infection Unit, Institut Pasteur, Paris, France.ORCID 0000-0001-5078-4083

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NK cells are important mediators of innate immunity and play an essential role for host protection against infection, although their responses to bacteria are poorly understood. Recently NK cells were shown to display memory properties, as characterized by an epigenetic signature leading to a stronger secondary response. Although NK cell memory could be a promising mechanism to fight against infection, it has not been described upon bacterial infection. Using a mouse model, we reveal that NK cells develop specific and long-term memory following sub-lethal infection with the extracellular pathogen Streptococcus pneumoniae. Memory NK cells display intrinsic sensing and response to bacteria in vitro, in a manner that is enhanced post-bacterial infection. In addition, their transfer into naïve mice confers protection from lethal infection for at least 12 weeks. Interestingly, NK cells display enhanced cytotoxic molecule production upon secondary stimulation and their protective role is dependent on Perforin and independent of IFNγ. Thus, our study identifies a new role for NK cells during bacterial infection, opening the possibility to harness innate immune memory for therapeutic purposes.

Indexed as

Killer Cells, NaturalStreptococcus pneumoniaeImmunity, InnatePerforinPerforin

Identifiers

PMID37486946
PMCPMC10399893

What OpenQuestion holds

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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.