Evidence map›Paper›PMID 25505487›Full record

ReviewFrontiers in genetics2014

Dysregulation of antiviral helicase pathways in systemic lupus erythematosus.

Luciana Oliveira, Nailú A Sinicato, Mariana Postal, Simone Appenzeller, Timothy B Niewold

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Molecular biology of autoinflammatory diseases.Inflammation and regeneration · 2021
    Review
  10. COVID-19 in patients with systemic lupus erythematosus: lessons learned from the inflammatory disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  11. Long noncoding RNA: TRIMming the viral load.Cellular & molecular immunology · 2019
    Article
  12. Review
  13. Type I interferon in rheumatic diseases.Nature reviews. Rheumatology · 2018
    Review
  14. Article
  15. Identification of Candidate Predictors of Lupus Flare.Transactions of the American Clinical and Climatological Association · 2015
    Review
  16. Review
  17. Helicases and human diseases.Frontiers in genetics · 2015
    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

5 authors at 1 institution in 1 country.

Luciana OliveiraRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas Campinas, Brazil.
Nailú A SinicatoRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas Campinas, Brazil.
Mariana PostalRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas Campinas, Brazil.
Simone AppenzellerRheumatology Unit, Department of Medicine, Faculty of Medical Science, State University of Campinas Campinas, Brazil.
Timothy B NiewoldMayo Clinic, Division of Rheumatology, Department of Immunology Rochester, MN, USA.
Mayo Clinic in Arizona · 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

In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primary pathogenic factor in the disease. Emerging evidence has implicated the antiviral helicases in this process. The antiviral helicases normally function as nucleic acid receptors in viral immunity. Genetic variations in antiviral helicase genes have been associated with SLE, supporting the idea that helicase pathways are involved in the primary pathogenesis of SLE. Studies have documented functional consequences of these genetic variations within the type I IFN pathway in human cell lines and SLE patients. In this review, we summarize the function of helicases in the anti-viral immune response, and how this response is dysregulated in SLE patients. In particular, we will focus on known functional genetic polymorphisms in the IFIH1 (MDA5) and mitochondrial antiviral signaling protein genes which have been implicated in human SLE. These data provide fascinating evidence for dysregulation of helicase-mediated innate immunity in SLE, and may support novel therapeutic strategies in the disease.

Indexed as

antiviral helicaseinterferonsystemic lupus erythematosus

Identifiers

PMID25505487
PMCPMC4243696
OpenAlexW2081363673

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.