Evidence map›Paper›PMID 26320138›Full record

ArticleRheumatology (Oxford, England)2016

Ankylosing spondylitis patients display altered dendritic cell and T cell populations that implicate pathogenic roles for the IL-23 cytokine axis and intestinal inflammation.

Pamela B Wright, Anne McEntegart, David McCarey, Iain B McInnes, Stefan Siebert, Simon W F Milling

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Efficacy and Safety of Curcumin andFrontiers in immunology · 2022
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Spondyloarthritides: Theories and beyond.Frontiers in pediatrics · 2022
    Review
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  9. Review
  10. Review
  11. Article
  12. Article
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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

6 authors at 2 institutions in 1 country.

Pamela B WrightInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow and.
Anne McEntegartDepartment of Rheumatology, Queen Elizabeth Building, Glasgow Royal Infirmary, Glasgow, UK.
David McCareyInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow and.
Iain B McInnesInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow and.
Stefan SiebertInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow and.
Simon W F MillingInstitute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow and simon.milling@glasgow.ac.uk.
University of Glasgow · GBGlasgow Royal Infirmary · GB

Funding

Arthritis Research UK 19853Chief Scientist Office ETM/304Versus Arthritis 19853Versus Arthritis 20816
6 · The paper itself

Abstract

objectiveAS is a systemic inflammatory disease of the SpA family. Polymorphisms at loci including HLA-B27, IL-23R and ERAP-1 directly implicate immune mechanisms in AS pathogenesis. Previously, in an SpA model, we identified HLA-B27-mediated effects on dendritic cells that promoted disease-associated Th17 cells. Here we extend these studies to AS patients using deep immunophenotyping of candidate pathogenic cell populations. The aim of our study was to functionally characterize the immune populations mediating AS pathology.

methodsUsing 11-parameter flow cytometry, we characterized the phenotype and functions of lymphocyte and myeloid cells from peripheral blood, and the synovial phenotype of AS patients and age-matched healthy controls.

resultsSignificantly fewer circulating CD1c-expressing dendritic cells were observed in AS patients, offset by an increase in CD14(-) CD16(+) mononuclear cells. Ex vivo functional analysis revealed that this latter population induced CCR6 expression and promoted secretion of IL-1β and IL-6 when co-cultured with naive CD4(+) T cells. Additionally, systemic inflammation in AS patients significantly correlated with increased proportions of activated CCR9(+) CD4(+) T cells.

conclusionCD14(-) CD16(+) mononuclear cells may contribute to AS by promoting Th17 responses, and antigen-presenting cells of mucosal origin are likely to contribute to systemic inflammation in AS.

Indexed as

Immunity, CellularPolymorphism, GeneticAdultAnimalsDendritic CellsDNAFemaleFlow CytometryHumansInflammationInterleukin-23MaleMiddle AgedRatsReal-Time Polymerase Chain ReactionRetrospective StudiesDNAInterleukin-23ankylosing spondylitisCD14− CD16+ mononuclear cellsCD4+ T cellsdendritic cellsinflammation

Identifiers

PMID26320138
PMCPMC4676904
OpenAlexW2162608009

What OpenQuestion holds

Textmetadata
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.