Evidence map›Paper›PMID 24907379›Full record

ReviewJournal of immunology (Baltimore, Md. : 1950)2014

Type I interferon in the pathogenesis of lupus.

Mary K Crow

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
326citing papers in PubMed, 9 pooled it
23.7field-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

326 citing papers in PubMed, 9 syntheses or guidelines pooled it, 556 citations in OpenAlex.

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  7. Guideline
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266 more citing papers are in PubMed but not listed here.

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.

Mary K CrowMary Kirkland Center for Lupus Research, Hospital for Special Surgery, New York, NY 10021; and Rheumatology Division, Department of Medicine, NewYork-Presbyterian/Weill Cornell Medical Center, New York, NY 10065 crowm@hss.edu.
Hospital for Special Surgery · US

Funding

RHEUMATOLOGY TRAININGT32AR007517 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 1986 to 2014
$2.2M
Interferon in Systemic Lupus ErythematosusR01AI059893 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 2006 to 2010
$2.1M
NIAID NIH HHS AI059893NIAID NIH HHS R01 AI059893NIAMS NIH HHS T32 AR007517
6 · The paper itself

Abstract

Investigations of patients with systemic lupus erythematosus have applied insights from studies of the innate immune response to define IFN-I, with IFN-α as the dominant mediator, as central to the pathogenesis of this prototype systemic autoimmune disease. Genetic association data identify regulators of nucleic acid degradation and components of TLR-independent, endosomal TLR-dependent, and IFN-I-signaling pathways as contributors to lupus disease susceptibility. Together with a gene expression signature characterized by IFN-I-induced gene transcripts in lupus blood and tissue, those data support the conclusion that many of the immunologic and pathologic features of this disease are a consequence of a persistent self-directed immune reaction driven by IFN-I and mimicking a sustained antivirus response. This expanding knowledge of the role of IFN-I and the innate immune response suggests candidate therapeutic targets that are being tested in lupus patients.

Indexed as

Immunity, InnateAnimalsGene Expression RegulationHumansInterferon Type ILupus Erythematosus, SystemicToll-Like ReceptorsInterferon Type IToll-Like Receptors

Identifiers

PMID24907379
PMCPMC4083591
OpenAlexW1896868877

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.