Evidence map›Paper›PMID 35143620›Full record

ArticleRheumatology (Oxford, England)2022

Gene signature fingerprints stratify SLE patients in groups with similar biological disease profiles: a multicentre longitudinal study.

M Javad Wahadat, Dieneke Schonenberg-Meinema, Cornelia G van Helden-Meeuwsen, Sander J van Tilburg, Noortje Groot, Ellen J H Schatorjé, Esther P A H Hoppenreijs, Petra C E Hissink Muller, Danielle M C Brinkman, Denis Dvorak and 5 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Rheumatology (Oxford, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Lupus nephritis.Nature reviews. Disease primers · 2025
    Review
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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

15 authors at 5 institutions in 2 countries.

M Javad WahadatDepartment of Immunology, Erasmus MC.ORCID 0000-0003-3961-1274
Dieneke Schonenberg-MeinemaDepartment of Pediatric Immunology, Rheumatology and Infectious diseases, Emma Children's Hospital, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.ORCID 0000-0001-9416-6631
Cornelia G van Helden-MeeuwsenDepartment of Immunology, Erasmus MC.
Sander J van TilburgDepartment of Immunology, Erasmus MC.
Noortje GrootDepartment of Paediatric Rheumatology, Erasmus MC-Sophia Children's hospital, University Medical Center Rotterdam, Rotterdam.ORCID 0000-0002-4711-0472
Ellen J H SchatorjéDepartment of Paediatric Rheumatology, Amalia Children's Hospital, Radboudumc.
Esther P A H HoppenreijsDepartment of Paediatric Rheumatology, Amalia Children's Hospital, Radboudumc.
Petra C E Hissink MullerDepartment of Pediatrics, Division of Pediatric Rheumatology, Willem Alexander Children's Hospital, Leiden University Medical Center, Leiden, The Netherlands.
Danielle M C BrinkmanDepartment of Pediatrics, Division of Pediatric Rheumatology, Willem Alexander Children's Hospital, Leiden University Medical Center, Leiden, The Netherlands.
Denis DvorakPaediatric Rheumatology, Department of Paediatrics, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic.
Marleen VerkaaikDepartment of Paediatric Rheumatology, Erasmus MC-Sophia Children's hospital, University Medical Center Rotterdam, Rotterdam.
J Merlijn van den BergDepartment of Pediatric Immunology, Rheumatology and Infectious diseases, Emma Children's Hospital, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Kateřina BouchalovaPaediatric Rheumatology, Department of Paediatrics, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic.ORCID 0000-0003-0175-7921
Sylvia KamphuisDepartment of Paediatric Rheumatology, Erasmus MC-Sophia Children's hospital, University Medical Center Rotterdam, Rotterdam.ORCID 0000-0002-1964-352X
Marjan A VersnelDepartment of Immunology, Erasmus MC.ORCID 0000-0003-0245-5386
Erasmus MC · NLAmalia Kinderziekenhuis · NLEmma Kinderziekenhuis · NLLeiden University Medical Center · NLUniversity Hospital Olomouc · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesClinical phenotyping and predicting treatment responses in SLE patients is challenging. Extensive blood transcriptional profiling has identified various gene modules that are promising for stratification of SLE patients. We aimed to translate existing transcriptomic data into simpler gene signatures suitable for daily clinical practice.

methodsReal-time PCR of multiple genes from the IFN M1.2, IFN M5.12, neutrophil (NPh) and plasma cell (PLC) modules, followed by a principle component analysis, was used to identify indicator genes per gene signature. Gene signatures were measured in longitudinal samples from two childhood-onset SLE cohorts (n = 101 and n = 34, respectively), and associations with clinical features were assessed. Disease activity was measured using Safety of Estrogen in Lupus National Assessment (SELENA)-SLEDAI. Cluster analysis subdivided patients into three mutually exclusive fingerprint-groups termed (1) all-signatures-low, (2) only IFN high (M1.2 and/or M5.12) and (3) high NPh and/or PLC.

resultsAll gene signatures were significantly associated with disease activity in cross-sectionally collected samples. The PLC-signature showed the highest association with disease activity. Interestingly, in longitudinally collected samples, the PLC-signature was associated with disease activity and showed a decrease over time. When patients were divided into fingerprints, the highest disease activity was observed in the high NPh and/or PLC group. The lowest disease activity was observed in the all-signatures-low group. The same distribution was reproduced in samples from an independent SLE cohort.

conclusionsThe identified gene signatures were associated with disease activity and were indicated to be suitable tools for stratifying SLE patients into groups with similar activated immune pathways that may guide future treatment choices.

Indexed as

Lupus Erythematosus, SystemicTranscriptomeChildCluster AnalysisGene Regulatory NetworksHumansLongitudinal Studiesbiomarkerschildhood-onset SLEclustering analysisdisease activitygene signaturesinterferonneutrophilsplasma cells

Identifiers

PMID35143620
PMCPMC9629374
OpenAlexW4210274015

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.