Evidence map›Paper›PMID 26882897›Full record

ArticleArthritis research & therapy2016

Physiological evidence for diversification of IFNα- and IFNβ-mediated response programs in different autoimmune diseases.

Tamarah D de Jong, Saskia Vosslamber, Elise Mantel, Sander de Ridder, John G Wesseling, Tineke C T M van der Pouw Kraan, Cyra Leurs, Harald Hegen, Florian Deisenhammer, Joep Killestein and 10 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 3 pooled it
4.2field-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

21 citing papers in PubMed, 3 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Role of IFN-α in Rheumatoid Arthritis.Current rheumatology reports · 2024
    Review
  8. Immunomodulatory Role of Interferons in Viral and Bacterial Infections.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Type I interferon in rheumatic diseases.Nature reviews. Rheumatology · 2018
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

20 authors at 5 institutions in 4 countries.

Tamarah D de JongDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. td.dejong@vumc.nl.
Saskia VosslamberDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. s.vosslamber@vumc.nl.
Elise MantelDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. e.mantel@vumc.nl.
Sander de RidderDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. s.deridder@vumc.nl.
John G WesselingDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. j.g.wesseling@durrercenter.nl.
Tineke C T M van der Pouw KraanDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands. t.vanderpouwkraan@vumc.nl.
Cyra LeursDepartment of Neurology, VU University Medical Center, Amsterdam, The Netherlands. c.leurs@vumc.nl.
Harald HegenDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. harald.hegen@i-med.ac.at.
Florian DeisenhammerDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Florian.Deisenhammer@tirol-kliniken.at.
Joep KillesteinDepartment of Neurology, VU University Medical Center, Amsterdam, The Netherlands. j.killestein@vumc.nl.
Ingrid E LundbergRheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden. Ingrid.Lundberg@ki.se.
Jiri VencovskyInstitute of Rheumatology, Prague, Czech Republic. vencovsky@revma.cz.
Mike T NurmohamedDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands. m.nurmohamed@reade.nl.
Dirkjan van SchaardenburgDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands. d.v.schaardenburg@reade.nl.
Irene E M BultinkDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, VUmc, Amsterdam, The Netherlands. IEM.Bultink@vumc.nl.
Alexandre E VoskuylDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, VUmc, Amsterdam, The Netherlands. AE.Voskuyl@vumc.nl.
D Michiel PegtelDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. d.pegtel@vumc.nl.
Conny J van der LakenDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, VUmc, Amsterdam, The Netherlands. J.vanderLaken@vumc.nl.
Johannes W J BijlsmaDepartment of Rheumatology, Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands. j.bijlsma@vumc.nl.
Cornelis L VerweijDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. c.verweij@vumc.nl.
Amsterdam UMC Location VUmc · NLInnsbruck Medical University · ATReade · NLInstitute of Rheumatology · CZKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of the type I interferon (IFN) response program is described for several autoimmune diseases, including systemic lupus erythematosus (SLE), multiple sclerosis (MS), myositis (IIM) and rheumatoid arthritis (RA). While IFNα contributes to SLE pathology, IFNβ therapy is often beneficial in MS, implying different immunoregulatory roles for these IFNs. This study was aimed to investigate potential diversification of IFNα-and IFNβ-mediated response programs in autoimmune diseases.

methodsPeripheral blood gene expression of 23 prototypical type I IFN response genes (IRGs) was determined in 54 healthy controls (HCs), 69 SLE (47 test, 22 validation), 149 IFNβ-treated MS (71 test, 78 validation), 160 untreated MS, 78 IIM and 76 RA patients. Patients with a type I IFN signature were selected for analysis.

resultsWe identified IFNα- and IFNβ-specific response programs (GC-A and GC-B, respectively) in SLE and IFNβ-treated MS patients. Concordantly, the GC-A/GC-B log-ratio was positive for all SLE patients and negative for virtually all IFNβ-treated MS patients, which was confirmed in additional cohorts. Applying this information to other autoimmune diseases, IIM patients displayed positive GC-A/GC-B log-ratios, indicating predominant IFNα activity. The GC-A/GC-B log-ratio in RA was lower and approached zero in part of the patients, implying relative importance of both clusters. Remarkably, GC-A/GC-B log-ratios appeared most heterogeneous in untreated MS; half of the patients displayed GC-A dominance, whereas others showed GC-B dominance or log-ratios near zero.

conclusionsOur findings show diversification of the type I IFN response in autoimmune diseases, suggesting different pathogenic roles of the type I IFNs.

Indexed as

AdultAgedAutoimmune DiseasesFemaleHumansInterferon-alphaInterferon-betaLupus Erythematosus, SystemicMaleMiddle AgedMultiple SclerosisTreatment OutcomeInterferon-alphaInterferon-beta

Identifiers

PMID26882897
PMCPMC4756531
OpenAlexW2282800417

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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.