Evidence map›Paper›PMID 16775617›Full record

ArticleGenes and immunity2006

Association of two functional polymorphisms in the CCR5 gene with juvenile rheumatoid arthritis.

S Prahalad, J F Bohnsack, L B Jorde, A Whiting, B Clifford, D Dunn, R Weiss, M Moroldo, S D Thompson, D N Glass and 1 more

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Genes and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00090571 (Research Registry for Juvenile Arthritis), which is not on this map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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.

NCT00090571 completednot on this map

Research Registry for Juvenile Arthritis

TypeobservationalSponsorNational Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)Ran1994 to 2009Enrolled200ConditionsJuvenile Rheumatoid Arthritis
3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

S PrahaladDivision of Immunology and Rheumatology, Department of Pediatrics, University of Utah, Salt Lake City, UT 84132-2206, USA. prahal@genetics.utah.edu
J F Bohnsack
L B Jorde
A Whiting
B Clifford
D Dunn
R Weiss
M Moroldo
S D Thompson
D N Glass
M J Bamshad
University of Utah · USCincinnati Children's Hospital Medical Center · USUniversity of Washington · US

Funding

VIRAL DAMAGE TO BRAIN AND NEUROMUSCULAR SYSTEMM01RR000064 · NCRR · UNIVERSITY OF UTAH · PI LEPPERT, MARK · 1985 to 2008
$21.7M
Pediatric Rheumatology Tissue RepostoryP01AR048929 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2003 to 2015
$13.6M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI WAGNER, MICHAEL · 2001 to 2015
$9.2M
Genetic variation in T-cell regulatory molecules and JRAK23AR050177 · NIAMS · UNIVERSITY OF UTAH · PI PRAHALAD, SAMPATH · 2004 to 2008
$674k
NCRR NIH HHS M01 RR000064NCRR NIH HHS M01-RR-00064NHLBI NIH HHS N01 AR042272NIAMS NIH HHS K23 AR050177NIAMS NIH HHS K23-AR-50177NIAMS NIH HHS N01-AR-42272NIAMS NIH HHS P01 AR048929NIAMS NIH HHS P01-AR-048929NIAMS NIH HHS P30 AR047363NIAMS NIH HHS P30-AR-47363
6 · The paper itself

Abstract

Juvenile rheumatoid arthritis (JRA) is mediated by Th1-immune responses. In children with JRA, synovial T cells express high levels of the Th1-chemokine receptor CC chemokine receptor 5 (CCR5), which has been implicated in susceptibility to rheumatoid arthritis. To test the hypothesis that genetic variation in CCR5 is associated with susceptibility to JRA, we analyzed patterns of variation in the 5'cis-regulatory region of CCR5 in 124 multiplex families from a JRA-affected sibpair registry. After sequencing the upstream region of CCR5, variants were tested for association with JRA by transmission disequilibrium testing. A single nucleotide polymorphism, C-1835T, was significantly undertransmitted to children with early-onset JRA (P<0.01). C-1835T was genotyped in 424 additional simplex and multiplex families. CCR5-1835T allele was undertransmitted in the cohort of all probands with JRA (P<0.02), as well as in those with early-onset (P<0.01) or pauciarticular JRA (P<0.05). Another variant, a 32-bp deletion in the open reading frame of CCR5 (CCR5-Delta32) was also tested in approximately 700 simplex and multiplex families. CCR5-Delta32 was also significantly undertransmitted to probands with early-onset JRA (P<0.05). Both variants are in regions under natural selection, and result in functional consequences. Our results suggest these CCR5 variants are protective against early-onset JRA.

Indexed as

Polymorphism, GeneticArthritis, JuvenileBase SequenceChildChild, PreschoolCohort StudiesFemaleGene DeletionGenetic Predisposition to DiseaseGenotypeHumansMalePolymorphism, Single NucleotideReceptors, CCR5Receptors, CCR5

Identifiers

PMID16775617
PMCPMC2927816
OpenAlexW2059646425

What OpenQuestion holds

Textmetadata
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Registered trials

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.