Evidence map›Paper›PMID 21859344›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2011

Type I interferon and systemic lupus erythematosus.

Keith B Elkon, Vivian V Stone

Open access · greenAbstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 3 pooled it
6.7field-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.

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

75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Article
  7. Article
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  10. Review
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  12. Article
  13. Basic Investigations in Pediatric Rheumatology.Indian journal of pediatrics · 2024
    Review
  14. Article
  15. MAVS Cys508 palmitoylation promotes its aggregation on the mitochondrial outer membrane and antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

15 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

2 authors at 1 institution in 1 country.

Keith B ElkonDivision of Rheumatology, University of Washington, Seattle, USA. elkon@u.washington.edu
Vivian V Stone
University of Washington · US

Funding

RESEARCH TRAINING IN RHEUMATOLOGYT32AR007108 · NIAMS · UNIVERSITY OF WASHINGTON · PI Shaun Jackson, Tomas M Mustelin · 1986 to 2026
$6.6M
Apoptotic Cells As Immunogens In SLER01AR048796 · NIAMS · UNIVERSITY OF WASHINGTON · PI ELKON, KEITH B. · 2001 to 2010
$2.7M
Agonists and Antagonists of Neuropsychiatric LupusR01NS065933 · NINDS · UNIVERSITY OF WASHINGTON · PI ELKON, KEITH B. · 2009 to 2012
$1.4M
NIAMS NIH HHS R01 AR48796NIAMS NIH HHS T32AR007108NINDS NIH HHS R01 NS065933
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease associated with multiple immunologic abnormalities. Prominent among these is upregulation of type I interferon (IFN)?a powerful immune adjuvant. IFN is, in part, produced in SLE in response to autoantigens in the form of self-nucleic acids and their associated nuclear proteins. Sources of these autoantigens include apoptotic and necrotic cells as well as neutrophils undergoing a specific form of cell death called NETosis. Although plasmacytoid dendritic cells are the main producers of IFN-a, other cells are important regulators of this process. Both genetic and environmental risk factors play a role in the development and pathogenesis of SLE. Further highlighting the importance of IFN, candidate gene and genome-wide association studies have identified a number of genes involved in type I IFN pathways associated with SLE. In this review, 3 monogenic deficiencies that result in lupus-like phenotypes and several polygenic variants that have been consistently associated with SLE are highlighted, and the relationship of these genes to IFN-a production is discussed. Clinical associations of the type I IFN pathway and the use of IFN-blocking agents as therapeutic agents in SLE are also reviewed.

Indexed as

Interferon Type ILupus Erythematosus, SystemicAnimalsHumansInterferon Type I

Identifiers

PMID21859344
PMCPMC3216059
OpenAlexW2061952755

What OpenQuestion holds

Textmetadata
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.