Evidence map›Paper›PMID 24109483›Full record

ReviewFrontiers in immunology2013

Nucleic Acid sensors and type I interferon production in systemic lupus erythematosus.

Meena Shrivastav, Timothy B Niewold

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
8.3field-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

58 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. CD8 T Cell Sensing of Type I Interferon Impacts Anergy.European journal of immunology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. CD11b agonists offer a novel approach for treating lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Meena ShrivastavDepartment of Rheumatology, Mayo Clinic , Rochester, MN , USA.
Timothy B Niewold
Mayo Clinic · US

Funding

Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
Genetic Regulation of interferon Alpha in Human LupusK08AI083790 · NIAID · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2009 to 2013
$616k
NIAID NIH HHS K08 AI083790NIAID NIH HHS L30 AI071651NIAMS NIH HHS R01 AR060861
6 · The paper itself

Abstract

The characteristic serologic feature of systemic lupus erythematosus (SLE) is autoantibodies against one's own nucleic acid or nucleic acid-binding proteins - DNA and RNA-binding nuclear proteins. Circulating autoantibodies can deposit in the tissue, causing inflammation and production of cytokines such as type 1 interferon (IFN). Investigations in human patients and animal models have implicated environmental as well as genetic factors in the biology of the SLE autoimmune response. Viral/Bacterial nucleic acid is a potent stimulant of innate immunity by both toll-like receptor (TLR) and non-TLR signaling cascades. Additionally, foreign DNA may act as an immunogen to drive an antigen-specific antibody response. Self nucleic acid is normally restricted to the nucleus or the mitochondria, away from the DNA/RNA sensors, and mechanisms exist to differentiate between foreign and self nucleic acid. In normal immunity, a diverse range of DNA and RNA sensors in different cell types form a dynamic and integrated molecular network to prevent viral infection. In SLE, pathologic activation of these sensors occurs via immune complexes consisting of autoantibodies bound to DNA or to nucleic acid-protein complexes. In this review, we will discuss recent studies outlining how mismanaged nucleic acid sensing networks promote autoimmunity and result in the over-production of type I IFN. This information is critical for improving therapeutic strategies for SLE disease.

Indexed as

DNAnucleic acid sensorRNAsystemic lupus erythematosusTLRtype 1 interferon

Identifiers

PMID24109483
PMCPMC3791549
OpenAlexW2019965289

What OpenQuestion holds

Textmetadata
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.