Evidence map›Paper›PMID 24587899›Full record

ReviewAutoimmune diseases2014

Genes associated with SLE are targets of recent positive selection.

Paula S Ramos, Stephanie R Shaftman, Ralph C Ward, Carl D Langefeld

Abstract readReview
In one paragraph

Review in Autoimmune diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Sez6L2 autoimmunity induces cerebellar ataxia in mice.Journal of neuroinflammation · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Lysosomes as a therapeutic target.Nature reviews. Drug discovery · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Population Genetics and Natural Selection in Rheumatic Disease.Rheumatic diseases clinics of North America · 2017
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  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

4 authors.

Paula S RamosDepartment of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Stephanie R ShaftmanDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Ralph C WardDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Carl D LangefeldDepartment of Public Health Sciences, Wake Forest School of Medicine and Center for Public Health Genomics, Winston-Salem, NC 27157, USA.

Funding

SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
South Carolina Clinical & Translational Research Institute (SCTR)UL1TR000062 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$9.4M
Patient Resource CoreP60AR062755 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SILVER, RICHARD M. · 2012 to 2016
$5.8M
NCATS NIH HHS UL1 TR000062NCRR NIH HHS UL1 RR029882NIAMS NIH HHS P60 AR062755
6 · The paper itself

Abstract

The reasons for the ethnic disparities in the prevalence of systemic lupus erythematosus (SLE) and the relative high frequency of SLE risk alleles in the population are not fully understood. Population genetic factors such as natural selection alter allele frequencies over generations and may help explain the persistence of such common risk variants in the population and the differential risk of SLE. In order to better understand the genetic basis of SLE that might be due to natural selection, a total of 74 genomic regions with compelling evidence for association with SLE were tested for evidence of recent positive selection in the HapMap and HGDP populations, using population differentiation, allele frequency, and haplotype-based tests. Consistent signs of positive selection across different studies and statistical methods were observed at several SLE-associated loci, including PTPN22, TNFSF4, TET3-DGUOK, TNIP1, UHRF1BP1, BLK, and ITGAM genes. This study is the first to evaluate and report that several SLE-associated regions show signs of positive natural selection. These results provide corroborating evidence in support of recent positive selection as one mechanism underlying the elevated population frequency of SLE risk loci and supports future research that integrates signals of natural selection to help identify functional SLE risk alleles.

Identifiers

PMID24587899
PMCPMC3920976

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Registered trials

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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.