Evidence map›Paper›PMID 23325834›Full record

ArticleBlood2013

NK cell responses to cytomegalovirus infection lead to stable imprints in the human KIR repertoire and involve activating KIRs.

Vivien Béziat, Lisa L Liu, Jenny-Ann Malmberg, Martin A Ivarsson, Ebba Sohlberg, Andreas T Björklund, Christelle Retière, Eva Sverremark-Ekström, James Traherne, Per Ljungman and 6 more

Open access · greenAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 313 papers.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed
23.6field-weighted citation impact, top 1% 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

313 citing papers in PubMed, 505 citations in OpenAlex.

  1. Trial
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  5. Trial
  6. Article
  7. Clonal selection of somatic mutations shapes NK cell memory.bioRxiv : the preprint server for biology · 2026
    Article
  8. Review
  9. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
  10. Article
  11. HLA-E-Directed Accumulation of KIRInternational journal of molecular sciences · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Resident CD49aScience advances · 2026
    Article
  20. Review

253 more citing papers are in PubMed but not listed here.

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

16 authors at 6 institutions in 4 countries.

Vivien BéziatCenter for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. vivien.beziat@ki.se
Lisa L Liu
Jenny-Ann Malmberg
Martin A Ivarsson
Ebba Sohlberg
Andreas T Björklund
Christelle Retière
Eva Sverremark-Ekström
James Traherne
Per Ljungman
Marie Schaffer
David A Price
John Trowsdale
Jakob Michaëlsson
Hans-Gustaf Ljunggren
Karl-Johan Malmberg
Karolinska Institutet · SEWenner-Gren Foundations · SECardiff University · GBKarolinska University Hospital · SENantes Université · FROslo University Hospital · NO

Funding

Medical Research CouncilWellcome Trust 100140
6 · The paper itself

Abstract

Human natural killer (NK) cells are functionally regulated by killer cell immunoglobulin-like receptors (KIRs) and their interactions with HLA class I molecules. As KIR expression in a given NK cell is genetically hard-wired, we hypothesized that KIR repertoire perturbations reflect expansions of unique NK-cell subsets and may be used to trace adaptation of the NK-cell compartment to virus infections. By determining the human "KIR-ome" at a single-cell level in more than 200 donors, we were able to analyze the magnitude of NK cell adaptation to virus infections in healthy individuals. Strikingly, infection with human cytomegalovirus (CMV), but not with other common herpesviruses, induced expansion and differentiation of KIR-expressing NK cells, visible as stable imprints in the repertoire. Education by inhibitory KIRs promoted the clonal-like expansion of NK cells, causing a bias for self-specific inhibitory KIRs. Furthermore, our data revealed a unique contribution of activating KIRs (KIR2DS4, KIR2DS2, or KIR3DS1), in addition to NKG2C, in the expansion of human NK cells. These results provide new insight into the diversity of KIR repertoire and its adaptation to virus infection, suggesting a role for both activating and inhibitory KIRs in immunity to CMV infection.

Indexed as

Cell DivisionCytomegalovirus InfectionsFlow CytometryHerpesviridae InfectionsHistocompatibility TestingHumansImmunophenotypingKiller Cells, NaturalLymphocyte ActivationNK Cell Lectin-Like Receptor Subfamily CReceptors, KIRReceptors, KIR3DS1KIR2DS2 protein, humanKIR2DS4 protein, humanKLRC2 protein, humanNK Cell Lectin-Like Receptor Subfamily CReceptors, KIRReceptors, KIR3DS1

Identifiers

PMID23325834
PMCPMC3617633
OpenAlexW2043570079

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.