Evidence map›Paper›PMID 30645688›Full record

ReviewCurrent rheumatology reports2019

Genetic Versus Non-genetic Drivers of SLE: Implications of IRF5 Dysregulation in Both Roads Leading to SLE.

Betsy J Barnes

Open access · greenAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

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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.

Betsy J BarnesCenter for Autoimmune Musculoskeletal and Hematopoietic Diseases, Northwell Health, Feinstein Institute for Medical Research, Hofstra-Northwell School of Medicine, 350 Community Dr, Hempstead, NY, 11030, USA. bbarnes1@northwell.edu.
Feinstein Institute for Medical Research · 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
NIAMS NIH HHS R21 AR065959
6 · The paper itself

Abstract

purpose of reviewSystemic lupus erythematosus (SLE) is characterized by a breakdown of immune tolerance, resulting in inflammation and tissue destruction. While the primary causes of SLE are still obscure, the disorder is highly heritable. Genetic risk variants, on their own, are rarely causal or fully explain disease pathogenesis. We discuss the possibility that IRF5, a SLE susceptibility gene, has both genetic and non-genetic contributions to disease pathogenesis. RECENT

findingsGenetic variants within and around IRF5 robustly associate with SLE risk. In SLE blood cells, IRF5 risk variants associate with elevated IRF5 expression and IFN production. Whether the observed increase in expression is due to risk variants or other disease-associated factors is not clear. Data from Irf5

Indexed as

AnimalsGene Expression RegulationGenetic Predisposition to DiseaseHumansInterferon Regulatory FactorsLupus Erythematosus, SystemicPolymorphism, Single NucleotideInterferon Regulatory FactorsIRF5 protein, humanGenotypeInterferonInterferon regulatory factorLupus

Identifiers

PMID30645688
PMCPMC11977172
OpenAlexW2910630164

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.