Evidence map›Paper›PMID 21575916›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2011

Interferon regulatory factors in human lupus pathogenesis.

Rafah Salloum, Timothy B Niewold

Abstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
12.0field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.

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  15. TheThe Indian journal of medical research · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Rafah SalloumSection of Rheumatology and Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA.
Timothy B Niewold
University of Chicago · US

Funding

ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI ABADIE, VALERIE · 1990 to 2025
$29.8M
TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Genetic Regulation of interferon Alpha in Human LupusK08AI083790 · NIAID · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2009 to 2013
$616k
NCRR NIH HHS UL1 RR024999NIAID NIH HHS AI071651NIAID NIH HHS AI083790NIAID NIH HHS K08 AI083790NIAID NIH HHS L30 AI071651NIDDK NIH HHS P30 DK042086NIDDK NIH HHS P30 DK42086
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a severe multisystem autoimmune disease that results from both genetic predisposition and environmental factors. Many lines of investigation support interferon alpha (IFN-α) as a causal agent in human lupus, and high levels of serum IFN-α are a heritable risk factor for SLE. Interferon regulatory factors (IRFs) are a family of transcription factors involved in host defense, which can induce transcription of IFN-α and other immune response genes after activation. In SLE, circulating immune complexes that contain nucleic acid are prevalent. These complexes are recognized by endosomal Toll-like receptors, resulting in activation of downstream IRF proteins. Genetic variants in the IRF5 and IRF7 genes have been associated with SLE susceptibility, and these same variants are associated with increased serum IFN-α in SLE patients. The increase in serum IFN-α related to IRF5 and 7 genotypes is observed only in patients with particular antibody specificities. This suggests that chronic stimulation of the endosomal Toll-like receptors by autoantibody immune complexes is required for IRF SLE-risk variants to cause elevation of circulating IFN-α and subsequent risk of SLE. Recently, genetic variation in the IRF8 gene has been associated with SLE and multiple sclerosis, and studies support an impact of IRF8 genotype on the IFN-α pathway. In summary, the SLE-associated polymorphisms in the IRF family of proteins seem to be gain-of-function variants, and understanding the impact of these variants on the IFN-α pathway in vivo may guide therapeutic strategies directed at the Toll-like receptor/IRF/IFN-α pathway in SLE.

Indexed as

AutoantibodiesGene ExpressionHumansInterferon-alphaInterferon Regulatory Factor-7Interferon Regulatory Factor-8Interferon Regulatory FactorsLupus Erythematosus, SystemicModels, BiologicalMultiple SclerosisPolymorphism, GeneticToll-Like ReceptorsTranslational Research, BiomedicalAutoantibodiesInterferon-alphaInterferon Regulatory Factor-7Interferon Regulatory Factor-8Interferon Regulatory FactorsIRF5 protein, humanIRF7 protein, humanToll-Like Receptors

Identifiers

PMID21575916
PMCPMC3096827
OpenAlexW2016758677

What OpenQuestion holds

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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.