Evidence map›Paper›PMID 30018803›Full record

ArticleRMD open2018

Expression analysis of HLA-E and NKG2A and NKG2C receptors points at a role for natural killer function in ankylosing spondylitis.

Alberto Cauli, Grazia Dessole, Matteo Piga, Maria Maddalena Angioni, Silvia Pinna, Alberto Floris, Mattia Congia, Enrico Mascia, Fabiana Paladini, Valentina Tedeschi and 3 more

Open access · goldAbstract read
In one paragraph

Article in RMD open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Biology of HLA class I associated inflammatory diseases.Best practice & research. Clinical rheumatology · 2024
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Dimorphism of HLA-E and its Disease Association.International journal of molecular sciences · 2019
    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

13 authors at 2 institutions in 1 country.

Alberto CauliRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Grazia DessoleRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Matteo PigaRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.ORCID 0000-0002-1126-8315
Maria Maddalena AngioniRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Silvia PinnaRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Alberto FlorisRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.ORCID 0000-0002-9154-0576
Mattia CongiaRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Enrico MasciaRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
Fabiana PaladiniDepartment of Biology and Biotechnologies 'Charles Darwin', Sapienza University of Rome, Rome, Italy.
Valentina TedeschiDepartment of Biology and Biotechnologies 'Charles Darwin', Sapienza University of Rome, Rome, Italy.
Rosa SorrentinoDepartment of Biology and Biotechnologies 'Charles Darwin', Sapienza University of Rome, Rome, Italy.
Maria Teresa FiorilloDepartment of Biology and Biotechnologies 'Charles Darwin', Sapienza University of Rome, Rome, Italy.
Alessandro MathieuRheumatology Unit, Department of Medical Sciences and Public Health, University of Cagliari, Cagliari, Italy.
University of Cagliari · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnkylosing spondylitis (AS) is a complex chronic inflammatory disease strongly associated with the majority of human leucocyte antigen (HLA)-B27 alleles. HLA-E molecules are non-classical major histocompatibility complex (MHC) class I molecules that specifically interact with the natural killer receptors NKG2A (inhibitory) and NKG2C (activating), and have been recently proposed to be involved in AS pathogenesis.''.

objectiveTo analyse the expression of HLA-E and the CD94/NKG2 pair of receptors in HLA-B27-positive patients with AS and healthy controls (HC) bearing the AS-associated B*2705 and the non-AS-associated B*2709 alleles.

methodsThe level of surface expression of HLA-E molecules on CD14+ peripheral blood mononuclear cell was evaluated in 21 HLA-B*2705 patients with AS, 12 HLA-B*2705 HC, 12 HLA-B*2709 HC and 6 HLA-B27-negative HC using the monoclonal antibody MEM-E/08 by quantitative cytofluorimetric analysis. The percentage and density of expression of HLA-E ligands NKG2A and NKG2C were also measured on CD3-CD56+ NK cells.

resultsHLA-E expression in CD14+ cells was significantly higher in patients with AS (587.0, IQR 424-830) compared with B*2705 HC (389, IQR 251.3-440.5; p=0.0007), B*2709 HC (294.5, IQR 209.5-422; p=0.0004) and HLA-B27-negative HC (380, IQR 197.3-515.0; p=0.01). A higher number of NK cells expressing NKG2A compared with NKG2C were found in all cohorts analysed, as well as a higher cell surface density.

conclusionThe higher surface level of HLA-E molecules in patients with AS compared with HC, concurrently with a prevalent expression of NKG2A, suggests that the crosstalk between these two molecules might play a role in AS pathogenesis, accounting for the previously reported association between HLA-E and AS.

Indexed as

ankylosing spondylitisinflammationspondyloarthritis

Identifiers

PMID30018803
PMCPMC6045714
OpenAlexW2883917546

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.