Evidence map›Paper›PMID 29348297›Full record

ArticleAnnals of the rheumatic diseases2018

Changes in macrophage transcriptome associate with systemic sclerosis and mediate

Aida Moreno-Moral, Marta Bagnati, Surya Koturan, Jeong-Hun Ko, Carmen Fonseca, Nathan Harmston, Laurence Game, Javier Martin, Voon Ong, David J Abraham and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 78 citations in OpenAlex.

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  5. Mechanistic insights into gasdermin-mediated pyroptosis.Nature reviews. Molecular cell biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Aida Moreno-Moral *Centre for Computational Biology, Duke-NUS Medical School, Singapore, Singapore.
Marta Bagnati *Centre for Complement and Inflammation Research, Hammersmith Hospital, Imperial College London, London, UK.
Surya KoturanCentre for Complement and Inflammation Research, Hammersmith Hospital, Imperial College London, London, UK.
Jeong-Hun KoCentre for Complement and Inflammation Research, Hammersmith Hospital, Imperial College London, London, UK.
Carmen FonsecaDivision of Medicine, Department of Inflammation, Centre for Rheumatology and Connective Tissue Diseases, Royal Free and University College Medical School, University College London, London, UK.
Nathan HarmstonCentre for Computational Biology, Duke-NUS Medical School, Singapore, Singapore.
Laurence GameGenomics Laboratory, MRC London Institute of Medical Sciences, Hammersmith Hospital, Imperial College London, London, UK.
Javier MartinInstituto de Parasitología y Biomedicina López Neyra, Consejo Superior de Investigaciones Cientıficas, Granada, Spain.
Voon OngDivision of Medicine, Department of Inflammation, Centre for Rheumatology and Connective Tissue Diseases, Royal Free and University College Medical School, University College London, London, UK.
David J AbrahamDivision of Medicine, Department of Inflammation, Centre for Rheumatology and Connective Tissue Diseases, Royal Free and University College Medical School, University College London, London, UK.
Christopher P DentonDivision of Medicine, Department of Inflammation, Centre for Rheumatology and Connective Tissue Diseases, Royal Free and University College Medical School, University College London, London, UK.
Jacques BehmoarasCentre for Complement and Inflammation Research, Hammersmith Hospital, Imperial College London, London, UK.
Enrico PetrettoCentre for Computational Biology, Duke-NUS Medical School, Singapore, Singapore.
The Royal Free Hospital · GBDuke-NUS Medical School · SGImperial College London · GBHammersmith Hospital · GBConsejo Superior de Investigaciones Científicas · ES

Funding

Arthritis Research UK 19427Medical Research Council MC_U120097112Medical Research Council MR/M004716/1Medical Research Council MR/N01121X/1Versus Arthritis 19427
6 · The paper itself

Abstract

objectivesSeveral common and rare risk variants have been reported for systemic sclerosis (SSc), but the effector cell(s) mediating the function of these genetic variants remains to be elucidated. While innate immune cells have been proposed as the critical targets to interfere with the disease process underlying SSc, no studies have comprehensively established their effector role. Here we investigated the contribution of monocyte-derived macrophages (MDMs) in mediating genetic susceptibility to SSc.

methodsWe carried out RNA sequencing and genome-wide genotyping in MDMs from 57 patients with SSc and 15 controls. Our differential expression and expression quantitative trait locus (eQTL) analysis in SSc was further integrated with epigenetic, expression and eQTL data from skin, monocytes, neutrophils and lymphocytes.

resultsWe identified 602 genes upregulated and downregulated in SSc macrophages that were significantly enriched for genes previously implicated in SSc susceptibility (P=5×10

conclusionsOur data further establish the link between macrophages and SSc, and suggest that the contribution of the rs3894194 risk variant to SSc susceptibility can be mediated by

Indexed as

Genetic Predisposition to DiseaseAdolescentAdultCase-Control StudiesChildChild, PreschoolFemaleGasderminsGenotyping TechniquesHumansMacrophagesMaleNeoplasm ProteinsQuantitative Trait LociRisk FactorsScleroderma, SystemicGasderminsGSDMA protein, humanNeoplasm ProteinseQTL analysisGSDMAmacrophagesystemic sclerosis

Identifiers

PMID29348297
PMCPMC5890626
OpenAlexW2783530444

What OpenQuestion holds

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Registered trials

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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.