Evidence map›Paper›PMID 15838509›Full record

ArticleNature genetics2005

A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities.

Yuta Kochi, Ryo Yamada, Akari Suzuki, John B Harley, Senji Shirasawa, Tetsuji Sawada, Sang-Cheol Bae, Shinya Tokuhiro, Xiaotian Chang, Akihiro Sekine and 13 more

Erratum issued Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Nature genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT00071175 (Lupus Genetic Studies; Lupus Family Registry & Repository), which is not on this map. Cited by 154 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 13 pooled it
13.4field-weighted citation impact, top 1% 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.

NCT00071175 completednot on this map

Lupus Genetic Studies; Lupus Family Registry & Repository

TypeobservationalSponsorOklahoma Medical Research FoundationRan1995 to 2013Enrolled3,460ConditionsSystemic Lupus Erythematosus
3 · Its place in the literature

Who cites it

154 citing papers in PubMed, 13 syntheses or guidelines pooled it, 409 citations in OpenAlex.

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  19. Association ofFrontiers in bioinformatics · 2026
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94 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

23 authors at 10 institutions in 3 countries.

Yuta KochiLaboratory for Rheumatic Diseases, SNP Research Center, RIKEN, Yokohama 230-0045, Japan.
Ryo Yamada
Akari Suzuki
John B Harley
Senji Shirasawa
Tetsuji Sawada
Sang-Cheol Bae
Shinya Tokuhiro
Xiaotian Chang
Akihiro Sekine
Atsushi Takahashi
Tatsuhiko Tsunoda
Yozo Ohnishi
Kenneth M Kaufman
Changsoo Paul Kang
Changwon Kang
Shigeru Otsubo
Wako Yumura
Akio Mimori
Takao Koike
Yusuke Nakamura
Takehiko Sasazuki
Kazuhiko Yamamoto
Institute for Rheumatic Diseases (Japan) · JPSaitama International Medical Center · JPThe University of Tokyo · JPKorea Advanced Institute of Science and Technology · KRHanyang University Seoul Hospital · KRHokkaido University · JPOklahoma City University · USOklahoma Medical Research Foundation · USRIKEN Center for Integrative Medical Sciences · JPTokyo Women's Medical University · JP

Funding

VALIDATING NOVEL GENES IMPLICATED IN LEUKOCYTE CHEMOTAXISP20RR020143 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GAFFNEY, PATRICK M · 2004 to 2011
$21.0M
Program Project in the Genetics of SLEP01AR049084 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIMBERLY, ROBERT P. · 2002 to 2012
$12.7M
HLA GENE COMPLEMENTATION IN PRIMARY SJOGREN'S AND LUPUSR01AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KOTTYAN, LEAH CLAIRE, WEIRAUCH, MATTHEW TYSON · 1987 to 2025
$7.8M
GENETIC ASSOCIATION WITH LUPUS IN AMERICAN BLACKSR01AR042460 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 1993 to 2009
$5.1M
Genetic Association in Sjogren's SyndromeR01DE015223 · NIDCR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2004 to 2008
$1.9M
NCRR NIH HHS P20 RR020143NIAID NIH HHS R01 AI024717NIAMS NIH HHS P01 AR049084NIAMS NIH HHS R01 AR042460NIDCR NIH HHS R01 DE015223
6 · The paper itself

Abstract

Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here we identify a SNP in the promoter region of FCRL3, a member of the Fc receptor-like family, that is associated with susceptibility to rheumatoid arthritis (odds ratio = 2.15, P = 0.00000085). This polymorphism alters the binding affinity of nuclear factor-kappaB and regulates FCRL3 expression. We observed high FCRL3 expression on B cells and augmented autoantibody production in individuals with the disease-susceptible genotype. We also found associations between the SNP and susceptibility to autoimmune thyroid disease and systemic lupus erythematosus. FCRL3 may therefore have a pivotal role in autoimmunity.

Indexed as

Arthritis, RheumatoidAutoimmunityCase-Control StudiesChromosomes, Human, Pair 1Gene Expression RegulationHLA-DR AntigensHLA-DRB1 ChainsHumansLinkage DisequilibriumMolecular Sequence DataMultigene FamilyMutationPolymorphism, Single NucleotideReceptors, ImmunologicFCRL3 protein, humanHLA-DR AntigensHLA-DRB1 ChainsReceptors, Immunologic

Identifiers

PMID15838509
PMCPMC1362949
OpenAlexW2170025624

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.