Evidence map›Paper›PMID 34563217›Full record

ReviewPediatric rheumatology online journal2021

JAK inhibitors: a potential treatment for JDM in the context of the role of interferon-driven pathology.

Meredyth G Ll Wilkinson, Claire T Deakin, Charalampia Papadopoulou, Despina Eleftheriou, Lucy R Wedderburn

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pediatric rheumatology online journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. 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

5 authors at 2 institutions in 2 countries.

Meredyth G Ll WilkinsonInfection, Immunity and Inflammation Programme Research and Teaching Department, UCL Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK. meredyth.wilkinson.14@ucl.ac.uk.ORCID http://orcid.org/0000-0002-7972-8066
Claire T DeakinInfection, Immunity and Inflammation Programme Research and Teaching Department, UCL Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Charalampia PapadopoulouInfection, Immunity and Inflammation Programme Research and Teaching Department, UCL Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Despina EleftheriouInfection, Immunity and Inflammation Programme Research and Teaching Department, UCL Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Lucy R WedderburnInfection, Immunity and Inflammation Programme Research and Teaching Department, UCL Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Great Ormond Street Hospital · GBArthritis UK · GB

Funding

CURE JM GOSH042019NIHR Great Ormond Street BRC 18IR33Versus Arthritis 20164 and 21593Versus Arthritis 21552
6 · The paper itself

Abstract

Juvenile Idiopathic Inflammatory Myopathies (IIM) are a group of rare diseases that are heterogeneous in terms of pathology that can include proximal muscle weakness, associated skin changes and systemic involvement. Despite options for treatment, many patients continue to suffer resistant disease and lasting side-effects. Advances in the understanding of the immunopathology and genetics underlying IIM may specify new therapeutic targets, particularly where conventional treatment has not achieved a clinical response. An upregulated type I interferon signature is strongly associated with disease and could be a prime target for developing more specific therapeutics. There are multiple components of the IFN pathway that could be targeted for blockade therapy.Downstream of the cytokine receptor complexes are the Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway, which consists of JAK1-3, TYK2, and STAT1-6. Therapeutic inhibitors have been developed to target components of this pathway. Promising results have been observed in case studies reporting the use of the JAK inhibitors, Baricitinib, Tofacitinib and Ruxolitinib in the treatment of refractory Juvenile Dermatomyositis (JDM). There is still the question of safety and efficacy for the use of JAK inhibitors in JDM that need to be addressed by clinical trials. Here we review the future for the use of JAK inhibitors as a treatment for JDM.

Indexed as

ChildDermatomyositisHumansInterferon Type IJanus Kinase InhibitorsInterferon Type IJanus Kinase InhibitorsIFNIIMJAK inhibitorsJAK/STAT pathwayJDMJuvenile dermatomyositisTreatment

Identifiers

PMID34563217
PMCPMC8466894
OpenAlexW3203976771

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.