Evidence map›Paper›PMID 31611734›Full record

ArticleMediators of inflammation2019

Altered Toll-Like Receptor Signalling in Children with Down Syndrome.

Dean Huggard, W J Koay, Lynne Kelly, Fiona McGrane, Emer Ryan, Niamh Lagan, Edna Roche, Joanne Balfe, T Ronan Leahy, Orla Franklin and 4 more

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  9. Congenital Heart Disease: An Immunological Perspective.Frontiers in cardiovascular medicine · 2021
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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

14 authors at 1 institution in 1 country.

Dean HuggardPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.ORCID https://orcid.org/0000-0002-0170-8399
W J KoayPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Lynne KellyPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Fiona McGranePaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Emer RyanPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Niamh LaganPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Edna RochePaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Joanne BalfePaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
T Ronan LeahyPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Orla FranklinPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Ana Moreno-OliveiraPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Ashanty M MeloPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.
Derek G DohertyPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.ORCID https://orcid.org/0000-0002-4394-658X
Eleanor J MolloyPaediatrics, Trinity College, The University of Dublin, Dublin, Ireland.ORCID https://orcid.org/0000-0001-6798-2158
Trinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are the key in initiating innate immune responses. TLR2 is crucial in recognising lipopeptides from gram-positive bacteria and is implicated in chronic inflammation. Children with Down syndrome (DS) are prone to infections from these pathogens and have an increased risk of autoimmunity. Sparstolonin B (SsnB) is a TLR antagonist which attenuates cytokine production and improves outcomes in sepsis. We hypothesised that TLR signalling may be abnormal in children with DS and contribute to their clinical phenotype. We evaluated TLR pathways in 3 ways: determining the expression of TLR2 on the surface of neutrophils and monocytes by flow cytometry, examining the gene expression of key regulatory proteins involved in TLR signal propagation, MyD88, IRAK4, and TRIF, by quantitative PCR, and lastly determining the cytokine production by ELISA following immunomodulation with proinflammatory stimuli (lipopolysaccharide (LPS), Pam3Csk4) and the anti-inflammatory agent SsnB. We report TLR2 expression being significantly increased on neutrophils, total monocytes, and intermediate and nonclassical monocytes in children with DS (

Indexed as

AdolescentAutoimmunityCD11b AntigenChildChild, PreschoolDown SyndromeEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHeterocyclic Compounds, 4 or More RingsHumansImmunity, InnateInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesMaleMonocytesCD11b AntigenHeterocyclic Compounds, 4 or More RingsInterleukin-1 Receptor-Associated KinasesIRAK4 protein, humanLipopolysaccharidessparstolonin BToll-Like Receptor 2Toll-Like Receptors

Identifiers

PMID31611734
PMCPMC6757445
OpenAlexW2973015423

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.