Evidence map›Paper›PMID 20220768›Full record

ArticleGenes and immunity2010

A candidate gene study of CLEC16A does not provide evidence of association with risk for anti-CCP-positive rheumatoid arthritis.

P G Bronson, P P Ramsay, M F Seldin, P K Gregersen, L A Criswell, L F Barcellos

Open access · greenAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Investigations of cellular immunity in juvenile idiopathic arthritis.Central-European journal of immunology · 2019
    Review
  2. 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

6 authors at 4 institutions in 1 country.

P G BronsonDivision of Epidemiology, School of Public Health, University of California, Berkeley, CA 94720-7356, USA.
P P Ramsay
M F Seldin
P K Gregersen
L A Criswell
L F Barcellos
University of California, Berkeley · USFeinstein Institute for Medical Research · USUniversity of California, Davis · USUniversity of California, San Francisco · US

Funding

ZD1839 FOR MALIGNANT ASTROCYTOMA OR GLIOBLASTOMA AND MENINGIOMAM01RR000079 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$26.0M
NARAC The Genetics of Rheumatoid ArthritisR01AR044422 · NIAMS · NORTH SHORE UNIVERSITY HOSPITAL · PI GREGERSEN, PETER K. · 1997 to 2011
$6.0M
Dissecting the HLA contribution to Rheumatoid ArthritisR01AI065841 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CRISWELL, LINDSEY ANN · 2006 to 2010
$3.2M
Admixture Mapping Development and Testing in AA SLER01AR050267 · NIAMS · UNIVERSITY OF CALIFORNIA DAVIS · PI SELDIN, MICHAEL F. · 2005 to 2009
$2.4M
Immunogenetic Studies of Autoimmune DiseaseR01AI059829 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARCELLOS, LISA F · 2004 to 2008
$1.9M
The Genetic Epidemiology of RA and SLEK24AR002175 · NIAMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CRISWELL, LINDSEY ANN · 2001 to 2005
$555k
Role of the MHC Class II tranactivator gene in lupus and rheumatoid arthritisF31AI075609 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BRONSON, PAOLA · 2008 to 2010
$81k
CONTINUATION OF THE GENETICS OF RHEUMATOID ARTHRITIS-264022263N01AR022263 · NIAMS · NORTH SHORE-LONG ISLAND JEWISH · 2002 to 2005
–
NCRR NIH HHS 5 M01 RR-00079NCRR NIH HHS M01 RR000079NIAID NIH HHS F31 AI075609NIAID NIH HHS R01 AI059829NIAID NIH HHS R01 AI065841NIAMS NIH HHS K24 AR002175NIAMS NIH HHS K24 AR02175NIAMS NIH HHS N01 AR022263NIAMS NIH HHS N01 AR22263NIAMS NIH HHS R01 AR044422NIAMS NIH HHS R01 AR050267NIAMS NIH HHS R01 AR44422Wellcome TrustWellcome Trust 076113
6 · The paper itself

Abstract

CLEC16A, a putative immunoreceptor, was recently established as a susceptibility locus for type I diabetes and multiple sclerosis. Subsequently, associations between CLEC16A and rheumatoid arthritis (RA), Addison's disease and Crohn's disease have been reported. A large comprehensive and independent investigation of CLEC16A variation in RA was pursued. This study tested 251 CLEC16A single-nucleotide polymorphisms in 2542 RA cases (85% anti-cyclic citrullinated peptide (anti-CCP) positive) and 2210 controls (N=4752). All individuals were of European ancestry, as determined by ancestry informative genetic markers. No evidence for significant association between CLEC16A variation and RA was observed. This is the first study to fully characterize common genetic variation in CLEC16A including assessment of haplotypes and gender-specific effects. The previously reported association between RA and rs6498169 was not replicated. Results show that CLEC16A does not have a prominent function in susceptibility to anti-CCP-positive RA.

Indexed as

AdultAgedAged, 80 and overArthritis, RheumatoidAutoantibodiesCohort StudiesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansLectins, C-TypeMaleMiddle AgedMonosaccharide Transport ProteinsPeptides, CyclicPolymorphism, Single NucleotideAutoantibodiesCLEC16A protein, humancyclic citrullinated peptideLectins, C-TypeMonosaccharide Transport ProteinsPeptides, Cyclic

Identifiers

PMID20220768
PMCPMC2992879
OpenAlexW1988715586

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.