Evidence map›Paper›PMID 15688186›Full record

SynthesisHuman genetics2005

CTLA-4 polymorphisms and systemic lupus erythematosus (SLE): a meta-analysis.

Young Ho Lee, John B Harley, Swapan K Nath

Registry-linked trialAbstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00071175 (Lupus Genetic Studies; Lupus Family Registry & Repository), which is not on this map. Cited by 51 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 11 pooled it
6.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 11 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  8. Associations between interleukin-23R polymorphisms and ankylosing spondylitis susceptibility: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Pooled it
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  12. Trial
  13. Review
  14. Narra J · 2025
    Article
  15. Article
  16. Immune Checkpoint Inhibitors and Lupus Erythematosus.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. 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 at 2 institutions in 1 country.

Young Ho LeeArthritis and Immunology Research Program, Oklahoma Medical Research Foundation, 825 N.E. 13th Street, Oklahoma City, OK 73104, USA.
John B Harley
Swapan K Nath
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

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 HARLEY, JOHN BARKER · 2002 to 2012
$12.7M
Trt. of Primary Hyperaldosteronism w/ACE Inhibitors &Angiotension Rec. BlockersM01RR014467 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TUCKER, PHEBE M · 2001 to 2007
$10.4M
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
THROMBOCYTOPENIA AND THE GENETICS OF SEVERE LUPUSP50AR048940 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI REICHLIN, MORRIS · 2002 to 2006
$5.8M
GENETIC ASSOCIATION WITH LUPUS IN AMERICAN BLACKSR01AR042460 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 1993 to 2009
$5.1M
Genetic Linkage in LupusR37AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2005 to 2014
$4.2M
Genetic Association in Sjogren's SyndromeR01DE015223 · NIDCR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2004 to 2008
$1.9M
Identifying the novel SLE susceptibility gene on 5p15.3R01AI063622 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI NATH, SWAPAN K. · 2005 to 2009
$1.5M
The first Sm epitopes in lupusR21AI053747 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2003 to 2004
$464k
Identifying the Vitiligo Related SLE Gene on 17p13R03AR048928 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI NATH, SWAPAN K · 2002 to 2004
$231k
LUPUS MULTIPLEX REGISTRY AND REPOSITORY-264012253N01AR012253 · NIAMS · OKLAHOMA MEDICAL RESEARCH FDN · 2002 to 2005
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NCRR NIH HHS RR01577NCRR NIH HHS RR020143NCRR NIH HHS RR14467NIAID NIH HHS AI053747NIAID NIH HHS AI063622NIAID NIH HHS AI24717NIAMS NIH HHS AR048928NIAMS NIH HHS AR049084NIAMS NIH HHS AR12253NIAMS NIH HHS AR42460NIAMS NIH HHS AR48940NIDCR NIH HHS DE15223
6 · The paper itself

Abstract

Several reports demonstrate association between variants of the cytotoxic T lymphocyte antigen-4 (CTLA-4) and autoimmune diseases. CTLA-4 may generate autoimmunity by immune dysregulation, making CTLA-4 an attractive candidate gene for systemic lupus erythematosus (SLE) susceptibility. Previous CTLA-4 association studies with SLE, however, have produced inconsistent results. We have performed a meta-analysis to better assess the purported associations. A total of 14 independent studies (to July 2004) testing association between one or more CTLA-4 polymorphisms and SLE were used in this analysis. We have compared allele and genotype frequencies at four polymorphic sites found in exon-1 (at +49), the promoter region (at -318 and -1722), and the 3' untranslated region (3'UTR) (dinucleotide repeat). We have evaluated both fixed and random effect models, depending on the presence of between-study heterogeneity. The data demonstrate that the exon-1 +49 polymorphism is significantly associated with SLE susceptibility. The overall risk, measured by odds ratio (OR), for exon-1 +49 GG genotype is 1.287 [95% confidence interval (CI)=1.031-1.562, P=0.011]. Stratification by ethnicity indicates the exon-1 +49 GG genotype is associated with SLE, at least in Asians (OR=1.293, 95% CI=1.031-1.620, P=0.026). European-derived populations have an effect of similar magnitude (OR=1.268, 95% CI=0.860-1.870, P=0.230), though not significant. Similar trends are found in allele-specific risk estimates and disease association. The OR for the exon-1 +49 risk allele (G) in Asians is 1.246 (95% CI=1.057-1.469, P=0.009), while Europeans have no evidence of allelic association (OR=0.978, 95% CI=0.833-1.148, P=0.780). In conclusion, this meta-analysis supports the CTLA-4 exon-1 +49 (A/G) polymorphism influencing the risk for developing SLE, especially in Asians.

Indexed as

Polymorphism, GeneticAntigens, CDAntigens, DifferentiationAsian PeopleCTLA-4 AntigenGene FrequencyGenetic Predisposition to DiseaseHumansLupus Erythematosus, SystemicAntigens, CDAntigens, DifferentiationCTLA-4 AntigenCTLA4 protein, human

Identifiers

PMID15688186
OpenAlexW2146283287

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.