Evidence map›Paper›PMID 19806151›Full record

ReviewNature reviews. Rheumatology2009

Oligoarticular and polyarticular JIA: epidemiology and pathogenesis.

Claudia Macaubas, Khoa Nguyen, Diana Milojevic, Jane L Park, Elizabeth D Mellins

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

73 citing papers in PubMed, 146 citations in OpenAlex.

  1. Trial
  2. Differential transcriptional and epigenetic signatures in CD4Journal of translational autoimmunity · 2026
    Article
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  7. Review
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  12. Assessment of choroidal vascularity index in juvenile idiopathic arthritis: implications for disease monitoring.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Article
  13. Article
  14. Review
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  20. Observational

13 more citing papers are in PubMed but not listed here.

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 1 country.

Claudia MacaubasDepartment of Pediatrics, Stanford University, Stanford, CA 94305-5164, USA.
Khoa Nguyen
Diana Milojevic
Jane L Park
Elizabeth D Mellins
Stanford University · USUniversity of California, San Francisco · US

Funding

Training Program in Adult and Pediatric RheumatologyT32AR050942 · NIAMS · STANFORD UNIVERSITY · PI LEWIS, DAVID BRAM, ROBINSON, WILLIAM H · 2005 to 2025
$6.6M
Immune cell dysfunction in SJIAR21AI075254 · NIAID · STANFORD UNIVERSITY · PI MELLINS, ELIZABETH D · 2008 to 2009
$435k
NIAID NIH HHS R21 AI075254NIAMS NIH HHS T32 AR050942
6 · The paper itself

Abstract

Juvenile idiopathic arthritis (JIA) refers to a group of chronic childhood arthropathies of unknown etiology, currently classified into subtypes primarily on the basis of clinical features. Research has focused on the hypothesis that these subtypes arise through distinct etiologic pathways. In this Review, we discuss four subtypes of JIA: persistent oligoarticular, extended oligoarticular, rheumatoid-factor-positive polyarticular and rheumatoid-factor-negative polyarticular. These subtypes differ in prevalence between ethnic groups and are associated with different HLA alleles. Non-HLA genetic risk factors have also been identified, some of which reveal further molecular differences between these subtypes, while others suggest mechanistic overlap. Investigations of immunophenotypes also provide insights into subtype differences: adaptive immunity seems to have a prominent role in both polyarticular and oligoarticular JIA, and the more-limited arthritis observed in persistent oligoarticular JIA as compared with extended oligoarticular JIA may reflect more-potent immunoregulatory T-cell activity in the former. Tumor necrosis factor seems to be a key mediator of both polyarticular and oligoarticular JIA, especially in the extended oligoarticular subtype, although elevated levels of other cytokines are also observed. Limited data on monocytes, dendritic cells, B cells, natural killer T cells and neutrophils suggest that the contributions of these cells differ across subtypes of JIA. Within each subtype, however, common pathways seem to drive joint damage.

Indexed as

Arthritis, JuvenileGenetic Predisposition to DiseaseAdaptive ImmunityGlobal HealthHumansMajor Histocompatibility ComplexMorbidityPhenotypeRisk Factors

Identifiers

PMID19806151
PMCPMC4159935
OpenAlexW1991586357

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.