Evidence map›Paper›PMID 27859049›Full record

ArticleImmunology2017

Lipopolysaccharide-primed heterotolerant dendritic cells suppress experimental autoimmune uveoretinitis by multiple mechanisms.

Izabela P Klaska, Elizabeth Muckersie, Cristina Martin-Granados, Maria Christofi, John V Forrester

Open access · hybridAbstract read
In one paragraph

Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Integrated network pharmacology andFrontiers in molecular biosciences · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. [Metformin and lipopolysaccharide regulate transcription ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Tolerance Induction in Relation to the Eye.Frontiers in immunology · 2018
    Review
  18. Anti-inflammatory Effects ofInternational journal of medical sciences · 2018
    Article
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

5 authors at 3 institutions in 2 countries.

Izabela P KlaskaInstitute of Ophthalmology, University College London, London, UK.
Elizabeth MuckersieInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Cristina Martin-GranadosInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Maria ChristofiInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
John V ForresterInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
University of Aberdeen · GBUniversity College London · GBUniversity of Western Australia · AU

Funding

Chief Scientist Office ETM/351
6 · The paper itself

Abstract

Exposure of bone-marrow-derived dendritic cells (BMDC) to high-dose ultrapure lipopolysaccharide for 24 hr (LPS-primed BMDC) enhances their potency in preventing inter-photoreceptor retinoid binding protein: complete Freund's adjuvant-induced experimental autoimmune uveoretinitis (EAU). LPS-primed BMDC are refractory to further exposure to LPS (= endotoxin tolerance), evidenced here by decreased phosphorylation of TANK-binding kinase 1, interferon regulatory factor 3 (IRF3), c-Jun N-terminal kinase and p38 mitogen-activated protein kinase as well as impaired nuclear translocation of nuclear factor κB (NF-κB) and IRF3, resulting in reduced tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-12 and interferon-β secretion. LPS-primed BMDC also show reduced surface expression of Toll-like receptor-4 and up-regulation of CD14, followed by increased apoptosis, mediated via nuclear factor of activated T cells (NFATc)-2 signalling. LPS-primed BMDC are not only homotolerant to LPS but are heterotolerant to alternative pathogen-associated molecular pattern ligands, such as mycobacterial protein extract (Mycobacterium tuberculosis). Specifically, while M. tuberculosis protein extract induces secretion of IL-1β, TNF-α and IL-6 in unprimed BMDC, LPS-primed BMDC fail to secrete these cytokines in response to M. tuberculosis. We propose that LPS priming of BMDC, by exposure to high doses of LPS for 24 hr, stabilizes their tolerogenicity rather than promoting immunogenicity, and does so by multiple mechanisms, namely (i) generation of tolerogenic apoptotic BMDC through CD14:NFATc signalling; (ii) reduction of NF-κB and IRF3 signalling and downstream pro-inflammatory cytokine production; and (iii) blockade of inflammasome activation.

Indexed as

AnimalsAutoimmune DiseasesBone Marrow CellsCells, CulturedCytokinesDendritic CellsImmune ToleranceInflammation MediatorsInterferon Regulatory Factor-3LipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutNFATC Transcription FactorsNF-kappa BRetinitisCytokinesInflammation MediatorsInterferon Regulatory Factor-3LipopolysaccharidesNfatc1 protein, mouseNFATC Transcription FactorsNF-kappa BTlr4 protein, mouseToll-Like Receptor 4dendritic cellsendotoxin toleranceexperimental autoimmune uveoretinitisheterotoleranceuveitis

Identifiers

PMID27859049
PMCPMC5290303
OpenAlexW2557147476

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.