Evidence map›Paper›PMID 21872224›Full record

ArticleCellular immunology2011

Targeting interferon regulatory factors to inhibit activation of the type I IFN response: implications for treatment of autoimmune disorders.

Susan E Sweeney

Open access · greenAbstract read
In one paragraph

Article in Cellular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Cellular FLIP long isoform (cFLIPThe Journal of biological chemistry · 2018
    Article
  6. Article
  7. Review
  8. Potentiation and tolerance of toll-like receptor priming in human endothelial cells.Translational research : the journal of laboratory and clinical medicine · 2017
    Article
  9. Article
  10. Review
  11. Article
  12. Genetics of the type I interferon pathway in systemic lupus erythematosus.International journal of clinical rheumatology · 2013
    Article
  13. Review
  14. 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

1 author at 1 institution in 1 country.

Susan E SweeneyDivision of Rheumatology, Allergy, and Immunology, University of California, San Diego, La Jolla, CA 92093, United States. ssweeney@ucsd.edu
University of California, San Diego · US

Funding

SAN DIEGO CLINICAL AND TRANSLATIONAL RESEARCH INSTITUTEUL1RR031980 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2010 to 2011
$14.0M
Regulation of the type I interferon response by IRFs in inflammatory arthritisR01AR059129 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2011 to 2015
$1.7M
Role of a novel IKK-related kinase in inflammationK08AR052800 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SWEENEY, SUSAN ELAINE · 2006 to 2010
$708k
NCRR NIH HHS 1UL1RR031980NCRR NIH HHS UL1 RR031980NIAMS NIH HHS K08 AR052800NIAMS NIH HHS R01 AR059129
6 · The paper itself

Abstract

The type I interferon (IFN) response plays a critical role in autoimmunity and is induced by innate receptor ligation and activation of IFN-regulatory factors (IRF). The present study investigated the roles and functional hierarchy of IRF3, IRF5, and IRF7 in expression of cytokines, chemokines, and matrix metalloproteinases in human THP1 monocytic cells. Targeted IRF knockdown was followed by evaluation of gene expression, promoter activation, and mRNA stability to determine the role of IRF as potential targets for modulating IFN responses in patients with autoimmune diseases. IRF played a distinct role in regulation of type I IFN gene expression in human monocytic cells and specifically regulated gene expression through the IFN-stimulated response element, with no contribution to transcription of traditionally AP-1 or NF-kB regulated genes. IRF7 regulated IL-6 gene expression by increasing IL-6 mRNA stability. IRF regulation of inflammation and induction of the IFN signature might contribute to the pathogenesis of autoimmune diseases and therefore represent novel therapeutic targets.

Indexed as

Autoimmune DiseasesCell LineGene Expression RegulationGene Knockdown TechniquesHumansInterferon Regulatory Factor-3Interferon Regulatory Factor-7Interferon Regulatory FactorsInterferon Type IInterleukin-6MonocytesPromoter Regions, GeneticRNA, Small InterferingRNA StabilityIL6 protein, humanInterferon Regulatory Factor-3Interferon Regulatory Factor-7Interferon Regulatory FactorsInterferon Type IInterleukin-6IRF3 protein, humanIRF5 protein, humanIRF7 protein, humanRNA, Small Interfering

Identifiers

PMID21872224
PMCPMC3248225
OpenAlexW1971873757

What OpenQuestion holds

Textmetadata
LicenceTDM
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.