Evidence map›Paper›PMID 31169548›Full record

ReviewCurrent opinion in rheumatology2019

Implications of juvenile idiopathic arthritis genetic risk variants for disease pathogenesis and classification.

Peter A Nigrovic, Marta Martínez-Bonet, Susan D Thompson

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Genetic association between theExperimental and therapeutic medicine · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Juvenile idiopathic arthritis.Nature reviews. Disease primers · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
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

3 authors.

Peter A NigrovicDivision of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital.
Marta Martínez-BonetDivision of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital.
Susan D ThompsonCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA.

Funding

Joint Biology Consortium Resource-based CenterP30AR070253 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter A Nigrovic, Jeffrey Andrew Sparks · 2016 to 2026
$9.4M
Tissue Repository CoreP30AR070549 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI Grant Sanford Schulert · 2016 to 2026
$7.7M
Ly6 family members in neutrophil biologyR01AR065538 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI NIGROVIC, PETER A · 2014 to 2024
$4.0M
Bridging the gap between GWAS and mechanism in JIAR01AR073201 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter A Nigrovic · 2019 to 2026
$3.2M
T resident memory cells in arthritisR01AR075906 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI NIGROVIC, PETER A · 2019 to 2023
$2.1M
NIAMS NIH HHS P30 AR070253NIAMS NIH HHS P30 AR070549NIAMS NIH HHS R01 AR065538NIAMS NIH HHS R01 AR073201NIAMS NIH HHS R01 AR075906
6 · The paper itself

Abstract

purpose of reviewWe assess the implications of recent advances in the genetics of juvenile idiopathic arthritis (JIA) for the evolving understanding of inflammatory arthritis in children. RECENT

findingsJIA exhibits prominent genetic associations with the human leukocyte antigen (HLA) region, extending perhaps surprisingly even to the hyperinflammatory systemic JIA category. Some HLA associations resemble those for adult-onset inflammatory arthritides, providing evidence for pathogenic continuity across the age spectrum. Genome-wide association studies have defined an increasing number of JIA-linked non-HLA loci, many again shared with adult-onset arthritis. As most risk loci contain only noncoding variants, new experimental methods such as SNP-seq and innovative big-data strategies help identify responsible causative mutations, termed functional SNPs (fSNPs). Alternately, gene hunting in multiplex families implicates new genes in monogenic childhood arthritis, including MYD88 and the intriguing innate immune gene LACC1. SUMMARY: Genetic data indicate a continuity between JIA and adult arthritis poorly reflected in current nomenclature. Advancing methodologies will help to identify new pathogenic mechanisms that inform the understanding of biologic subdivisions within JIA. Resulting insights will facilitate the application of lessons learned across the age spectrum to the treatment of arthritis in children and adults.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideArthritis, JuvenileGenome-Wide Association StudyHLA AntigensHumansRisk FactorsHLA Antigens

Identifiers

PMID31169548
PMCPMC6800096

What OpenQuestion holds

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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.