Evidence map›Paper›PMID 23826184›Full record

ArticlePloS one2013

SLE peripheral blood B cell, T cell and myeloid cell transcriptomes display unique profiles and each subset contributes to the interferon signature.

Amy M Becker, Kathryn H Dao, Bobby Kwanghoon Han, Roger Kornu, Shuchi Lakhanpal, Angela B Mobley, Quan-Zhen Li, Yun Lian, Tianfu Wu, Andreas M Reimold and 9 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 3 pooled it
9.1field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 3 syntheses or guidelines pooled it, 194 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. InterferonFrontiers in immunology · 2020
    Trial
  6. Review
  7. Article
  8. The multilayered identity of B cell memory.Cellular & molecular immunology · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Mutant p53Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

53 more citing papers are in PubMed but not listed here.

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

19 authors at 2 institutions in 1 country.

Amy M BeckerDepartment of Immunology, The University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Kathryn H Dao
Bobby Kwanghoon Han
Roger Kornu
Shuchi Lakhanpal
Angela B Mobley
Quan-Zhen Li
Yun Lian
Tianfu Wu
Andreas M Reimold
Nancy J Olsen
David R Karp
Fatema Z Chowdhury
J David Farrar
Anne B Satterthwaite
Chandra Mohan
Peter E Lipsky
Edward K Wakeland
Laurie S Davis
The University of Texas Southwestern Medical Center · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

SLAM Genes-from Mouse to ManP50AR055503 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI KARP, DAVID R · 2007 to 2011
$8.3M
TH-1 BIAS IN RHEUMATOID ARTHRITISR01AR045293 · NIAMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI DAVIS, LAURIE S · 1999 to 2003
$1.1M
NIAMS NIH HHS P50 AR055503NIAMS NIH HHS P50AR055503NIAMS NIH HHS R01 AR045293NIAMS NIH HHS R01AR45293
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that is characterized by defective immune tolerance combined with immune cell hyperactivity resulting in the production of pathogenic autoantibodies. Previous gene expression studies employing whole blood or peripheral blood mononuclear cells (PBMC) have demonstrated that a majority of patients with active disease have increased expression of type I interferon (IFN) inducible transcripts known as the IFN signature. The goal of the current study was to assess the gene expression profiles of isolated leukocyte subsets obtained from SLE patients. Subsets including CD19(+) B lymphocytes, CD3(+)CD4(+) T lymphocytes and CD33(+) myeloid cells were simultaneously sorted from PBMC. The SLE transcriptomes were assessed for differentially expressed genes as compared to healthy controls. SLE CD33(+) myeloid cells exhibited the greatest number of differentially expressed genes at 208 transcripts, SLE B cells expressed 174 transcripts and SLE CD3(+)CD4(+) T cells expressed 92 transcripts. Only 4.4% (21) of the 474 total transcripts, many associated with the IFN signature, were shared by all three subsets. Transcriptional profiles translated into increased protein expression for CD38, CD63, CD107a and CD169. Moreover, these studies demonstrated that both SLE lymphoid and myeloid subsets expressed elevated transcripts for cytosolic RNA and DNA sensors and downstream effectors mediating IFN and cytokine production. Prolonged upregulation of nucleic acid sensing pathways could modulate immune effector functions and initiate or contribute to the systemic inflammation observed in SLE.

Indexed as

AdultB-LymphocytesDNAFemaleGene Expression ProfilingHumansInterferonsLupus Erythematosus, SystemicMiddle AgedMyeloid CellsOligonucleotide Array Sequence AnalysisReproducibility of ResultsRNARNA, MessengerT-Lymphocyte SubsetsTranscriptomeDNAInterferonsRNARNA, Messenger

Identifiers

PMID23826184
PMCPMC3691135
OpenAlexW2072127157

What OpenQuestion holds

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LicenceCC BY
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.