Evidence map›Paper›PMID 24673109›Full record

Trial reportImmunology2014

Balance between activating NKG2D, DNAM-1, NKp44 and NKp46 and inhibitory CD94/NKG2A receptors determine natural killer degranulation towards rheumatoid arthritis synovial fibroblasts.

Natasja Nielsen, Veronique Pascal, Andreas E R Fasth, Yvonne Sundström, Elisabeth D Galsgaard, David Ahern, Martin Andersen, Bo Baslund, Else M Bartels, Henning Bliddal and 5 more

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. [Research progress of the ULBP-NKG2D axis in autoimmune diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Journal of personalized medicine · 2021
    Article
  10. Review
  11. Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021
    Review
  12. Article
  13. CD226: An Emerging Role in Immunologic Diseases.Frontiers in cell and developmental biology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

15 authors at 5 institutions in 3 countries.

Natasja NielsenDepartment of Translational Immunology, Novo Nordisk A/S, Måløv, Denmark.
Veronique Pascal
Andreas E R Fasth
Yvonne Sundström
Elisabeth D Galsgaard
David Ahern
Martin Andersen
Bo Baslund
Else M Bartels
Henning Bliddal
Marc Feldmann
Vivianne Malmström
Louise Berg
Pieter Spee
Kalle Söderström
Karolinska University Hospital · SENovo Nordisk (Denmark) · DKUniversity of Oxford · GBCopenhagen University Hospital · DKFrederiksberg Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and synovial hyperplasia leading to progressive joint destruction. Fibroblast-like synoviocytes (FLS) are central components of the aggressive, tumour-like synovial structure termed pannus, which invades the joint space and cartilage. A distinct natural killer (NK) cell subset expressing the inhibitory CD94/NKG2A receptor is present in RA synovial fluid. Little is known about possible cellular interactions between RA-FLS and NK cells. We used cultured RA-FLS and the human NK cell line Nishi, of which the latter expresses an NK receptor repertoire similar to that of NK cells in RA synovial fluid, as an in vitro model system of RA-FLS/NK cell cross-talk. We show that RA-FLS express numerous ligands for both activating and inhibitory NK cell receptors, and stimulate degranulation of Nishi cells. We found that NKG2D, DNAM-1, NKp46 and NKp44 are the key activating receptors involved in Nishi cell degranulation towards RA-FLS. Moreover, blockade of the interaction between CD94/NKG2A and its ligand HLA-E expressed on RA-FLS further enhanced Nishi cell degranulation in co-culture with RA-FLS. Using cultured RA-FLS and the human NK cell line Nishi as an in vitro model system of RA-FLS/NK cell cross-talk, our results suggest that cell-mediated cytotoxicity of RA-FLS may be one mechanism by which NK cells influence local joint inflammation in RA.

Indexed as

Antigens, Differentiation, T-LymphocyteArthritis, RheumatoidCell DegranulationCell LineFemaleFibroblastsHistocompatibility Antigens Class IHLA-E AntigensHumansKiller Cells, NaturalMaleNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 2NK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DNK Cell Lectin-Like Receptor Subfamily KAntigens, Differentiation, T-LymphocyteHistocompatibility Antigens Class IHLA-E AntigensKLRD1 protein, humanKLRK1 protein, humanNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 2NCR1 protein, humanNCR2 protein, humanNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DNK Cell Lectin-Like Receptor Subfamily KT Lineage-Specific Activation Antigen 1CD94/NKG2Afibroblast-like synoviocytesnatural killer cytotoxicityNKG2D

Identifiers

PMID24673109
PMCPMC4107668
OpenAlexW2044926090

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.