Evidence map›Paper›PMID 31130331›Full record

ReviewCytokine2020

Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis.

Bharati Matta, Betsy J Barnes

Registry-linked trialAbstract readReview
In one paragraph

Review in Cytokine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04558814 (Evaluation of Serum Galectin-9 Level in Systemic Lupus Erythematosus Patients and it's Association With Disease Activity and Organ Damage), which is not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-weighted citation impact, top 8% 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.

NCT04558814 naunknown statusnot on this mapstarted 2021, after this paper: background citation

Evaluation of Serum Galectin-9 Level in Systemic Lupus Erythematosus Patients and it's Association With Disease Activity and Organ Damage

TypeinterventionalSponsorAssiut UniversityRan2021 to 2022Enrolled100ConditionsSystemic Lupus ErythematosusArmsSerum galectin-9 level
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024
    Review
  11. Article
  12. Article
  13. Genetic association between theExperimental and therapeutic medicine · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Bharati MattaCenter for Autoimmune Musculoskeletal and Hematopoietic Diseases, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, USA.
Betsy J BarnesCenter for Autoimmune Musculoskeletal and Hematopoietic Diseases, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, USA; Departments of Molecular Medicine and Pediatrics, Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY 11549, USA. Electronic address: bbarnes1@northwell.edu.
Feinstein Institute for Medical Research · USNorthwell Health · US

Funding

IRF5-TNPO3 locus: Inclusion of TNPO3 as a unique regulator of IRF5 expression anR21AR065959 · NIAMS · RBHS-NEW JERSEY MEDICAL SCHOOL · PI BARNES, BETSY J · 2014 to 2015
$385k
ROLE OF IRF5 IN SLE PATHOGENESISR03AR054070 · NIAMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BARNES, BETSY J · 2006 to 2008
$227k
NIAMS NIH HHS R03 AR054070NIAMS NIH HHS R21 AR065959
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a complex autoimmune disease which affects multiple organs. The type I interferon (IFN) gene signature and circulating autoantibodies are hallmarks of SLE. Plasmacytoid dendritic cells (pDCs) are considered the main producers of type I IFN and production is modulated by multiple other immune cell types. In SLE, essentially every immune cell type is dysregulated and aberrant deregulation is thought to be due, in part, to direct or indirect exposure to IFN. Genetic variants within or around the transcription factor interferon regulatory factor 5 (IRF5) associate with SLE risk. Elevated IFNα activity was detected in the sera of SLE patients carrying IRF5 risk polymorphisms who were positive for either anti-RNA binding protein (anti-RBP) or anti-double-stranded DNA (anti-dsDNA) autoantibodies. Neutrophils are also an important source of type I IFNs and are found in abundance in human blood. Neutrophil extracellular traps (NETs) are considered a potential source of antigenic trigger in SLE that can lead to type I IFN gene induction, as well as increased autoantibody production. In this review, we will focus on immune cell types that produce type I IFNs and/or are affected by type I IFN in SLE. In addition, we will discuss potential inducers of endogenous type I IFN production in SLE. Last, we will postulate how the different immune cell populations may be affected by an IRF5-SLE risk haplotype.

Indexed as

B-LymphocytesDendritic CellsHumansImmunity, InnateInterferon Regulatory FactorsInterferon Type ILupus Erythematosus, SystemicNeutrophilsPolymorphism, GeneticT-LymphocytesInterferon Regulatory FactorsInterferon Type IIRF5 protein, humanAutoimmunityNETosisNeutrophilsPlasmacytoid dendritic cellsSLE

Identifiers

PMID31130331
PMCPMC11931518
OpenAlexW2946554594

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.