Evidence map›Paper›PMID 27906774›Full record

ReviewCurrent opinion in rheumatology2017

Lessons from characterization and treatment of the autoinflammatory syndromes.

Ivona Aksentijevich, Michael F McDermott

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-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

24 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
  3. Co-Occurrence ofInternational journal of molecular sciences · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Panniculitis: A Cardinal Sign of Autoinflammation.Current rheumatology reviews · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Rare Autoinflammatory Diseases.Turkish archives of pediatrics · 2022
    Article
  13. Article
  14. Overview of the rarest causes of fever in newborns: handy hints for the neonatologist.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Review
  15. Notch Signaling Regulation in Autoinflammatory Diseases.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Article
  18. The off-label use of anakinra in pediatric systemic autoinflammatory diseases.Therapeutic advances in musculoskeletal disease · 2020
    Review
  19. Article
  20. [Association between autophagy and systemic juvenile idiopathic arthritis and related mechanism: a preliminary study].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019
    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

2 authors at 2 institutions in 2 countries.

Ivona AksentijevichaInflammatory Disease Section, National Human Genome Research Institute, Bethesda, Maryland, USA bNIHR National Institute for Health Research-Leeds Musculoskeletal Biomedical Research Unit (NIHR-LMBRU) and Leeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), Wellcome Trust Brenner Building, St. James's University Hospital, Leeds, UK.
Michael F McDermott
GTx (United States) · USWellcome Trust · GB

Funding

Intramural NIH HHS Z99 HG999999
6 · The paper itself

Abstract

purpose of reviewThe list of genes associated with systemic inflammatory diseases has been steadily growing because of the explosion of new genomic technologies. Significant advances in the past year have deepened our understanding of the molecular mechanisms linked to inflammation and elucidated insights on the efficacy of specific therapies for these and related conditions. We review the molecular pathogenesis of four recently characterized monogenic autoinflammatory diseases: haploinsufficiency of A20, otulipenia, a severe form of pyrin-associated disease, and a monogenic form of systemic juvenile idiopathic arthritis. RECENT

findingsThe scope of autoinflammation has been broadened to include defects in deubiquitination and cellular redox homeostasis. At the clinical level, we discuss the biological rationale for treatment with cytokine inhibitors and colchicine in respective conditions and the use of interleukin-1 antagonism for diagnostic and therapeutic purposes in the management of undifferentiated autoinflammatory disorders. SUMMARY: Gene discoveries coupled with studies of molecular function provide knowledge into the biology of inflammatory responses and form the basis for genomically informed therapies. Diseases of dysregulated ubiquitination constitute a novel category of human inflammatory disorders.

Indexed as

Antirheumatic AgentsArthritis, JuvenileColchicineEndopeptidasesFamilial Mediterranean FeverHaploinsufficiencyHereditary Autoinflammatory DiseasesHumansInterleukin 1 Receptor Antagonist ProteinIntracellular Signaling Peptides and ProteinsMevalonate Kinase DeficiencyPhosphotransferases (Alcohol Group Acceptor)ProteinsPyrinTubulin ModulatorsTumor Necrosis Factor alpha-Induced Protein 3Antirheumatic AgentsColchicineEndopeptidasesInterleukin 1 Receptor Antagonist ProteinIntracellular Signaling Peptides and ProteinsLACC1 protein, humanMEFV protein, humanmevalonate kinaseOTULIN protein, humanPhosphotransferases (Alcohol Group Acceptor)ProteinsPyrinTNFAIP3 protein, humanTubulin ModulatorsTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID27906774
PMCPMC5823535
OpenAlexW2558307473

What OpenQuestion holds

Textmetadata
LicenceTDM
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.