Evidence map›Paper›PMID 25644502›Full record

ArticleClinical and experimental immunology2015

Phenotypical and functional profiles of natural killer cells exhibiting matrix metalloproteinase-mediated CD16 cleavage after anti-HIV antibody-dependent activation.

C-C Tang, G Isitman, J Bruneau, C Tremblay, N F Bernard, S J Kent, M S Parsons

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Role of NK Cells in Tumor Progression.Experientia supplementum (2012) · 2022
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Beyond Viral Neutralization.AIDS research and human retroviruses · 2017
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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

7 authors at 4 institutions in 2 countries.

C-C TangDepartment of Microbiology and Immunology, University of Melbourne, Peter Doherty Institute, Melbourne, Victoria, Australia.
G IsitmanResearch Institute of the McGill University Health Centre, McGill University, Montreal, Quebec, Canada.
J BruneauCentre de Recherche du Centre Hospitalier de l'Universite de Montreal (CRCHUM), Montreal, Quebec, Canada.
C TremblayCentre de Recherche du Centre Hospitalier de l'Universite de Montreal (CRCHUM), Montreal, Quebec, Canada.
N F BernardResearch Institute of the McGill University Health Centre, McGill University, Montreal, Quebec, Canada.
S J KentDepartment of Microbiology and Immunology, University of Melbourne, Peter Doherty Institute, Melbourne, Victoria, Australia.
M S ParsonsDepartment of Microbiology and Immunology, University of Melbourne, Peter Doherty Institute, Melbourne, Victoria, Australia.
Centre Hospitalier de l’Université de Montréal · CAMcGill University Health Centre · CAUniversity of Melbourne · AUPeter Doherty Institute · AU

Funding

Canadian Institutes of Health Research HOP-123800Canadian Institutes of Health Research MOP-111155Canadian Institutes of Health Research THA-118628
6 · The paper itself

Abstract

Natural killer (NK) cell-mediated antibody-dependent cellular cytotoxicity (ADCC) has been linked to protection from HIV infection and slower progression towards AIDS. However, antibody-dependent activation of NK cells results in phenotypical alterations similar to those observed on NK cells from individuals with progressive HIV infection. Activation of NK cells induces matrix metalloproteinase (MMP)-mediated cleavage of cell surface CD16. In the present study we assessed the phenotype and functional profile of NK cells exhibiting post-activation MMP-mediated CD16 cleavage. We found that NK cells achieving the highest levels of activation during stimulation exhibit the most profound decreases in CD16 expression. Further, we observed that educated KIR3DL1(+) NK cells from human leucocyte antigen (HLA)-Bw4-carrying donors exhibit larger decreases in CD16 expression post-activation than the KIR3DL1(-) NK cell subset containing cells educated via other inhibitory receptor/ligand combinations and non-educated NK cells. Lastly, we assessed the ex-vivo expression of CD16 on educated KIR3DL1(+) NK cells and the KIR3DL1(-) NK cell subset from HLA-Bw4-carrying HIV-uninfected and HIV-infected donors. Suggestive of in-vivo activation of KIR3DL1(+) NK cells during HIV infection, CD16 expression was higher on KIR3DL1(+) than KIR3DL1(-) NK cells in uninfected donors but similar on both subsets in HIV-infected donors. These results are discussed in the context of how they may assist with understanding HIV disease progression and the design of immunotherapies that utilize antibody-dependent NK cell responses.

Indexed as

AntibodiesAntibody-Dependent Cell CytotoxicityDisease ProgressionGene ExpressionGPI-Linked ProteinsHistocompatibility TestingHIV-1HIV InfectionsHLA-B AntigensHumansImmunophenotypingKiller Cells, NaturalLymphocyte ActivationMatrix MetalloproteinasesPhenotypePrimary Cell CultureAntibodiesFCGR3B protein, humanGPI-Linked ProteinsHLA-B AntigensHLA-Bw4 antigenKIR3DL1 protein, humanMatrix MetalloproteinasesReceptors, IgGReceptors, KIR3DL1RNA, ViralAIDSKIR3DL1NK cell education

Identifiers

PMID25644502
PMCPMC4516443
OpenAlexW1963115426

What OpenQuestion holds

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Registered trials

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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.