Evidence map›Paper›PMID 33246136›Full record

ReviewCurrent opinion in immunology2020

Type I interferon in the pathogenesis of systemic lupus erythematosus.

Mariana Postal, Jessica F Vivaldo, Ruth Fernandez-Ruiz, Jacqueline L Paredes, Simone Appenzeller, Timothy B Niewold

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 1 pooled it
17.7field-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

178 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.

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  13. The theory of the inflammatory ecosystem.Science China. Life sciences · 2026
    Review
  14. Autoantibodies neutralizing type I interferons underlie a third of cases of Chikungunya virus encephalitis or myelitis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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118 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

6 authors at 2 institutions in 2 countries.

Mariana PostalAutoimmunity Lab, School of Medical Science, State University of Campinas, Campinas, SP, Brazil.
Jessica F VivaldoAutoimmunity Lab, School of Medical Science, State University of Campinas, Campinas, SP, Brazil; Graduate Program of Child and Adolescent Health, School of Medical Science, State University of Campinas, Campinas, SP, Brazil.
Ruth Fernandez-RuizColton Center for Autoimmunity, New York University School of Medicine, New York, NY, USA.
Jacqueline L ParedesColton Center for Autoimmunity, New York University School of Medicine, New York, NY, USA.
Simone AppenzellerAutoimmunity Lab, School of Medical Science, State University of Campinas, Campinas, SP, Brazil; Rheumatology Unit, Department of Medicine, School of Medical Science, State University of Campinas, Campinas, SP, Brazil.
Timothy B NiewoldColton Center for Autoimmunity, New York University School of Medicine, New York, NY, USA. Electronic address: Timothy.Niewold@nyulangone.org.
New York University · USUniversidade Estadual de Campinas (UNICAMP) · BR

Funding

Interferon Regulatory Factor 5 in Human Lupus PathogenesisR01AR065964 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2015 to 2018
$2.0M
Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
The Role of IL-17 Axis in Inflammatory MyositisR01AR057781 · NIAMS · MAYO CLINIC ROCHESTER · PI NIEWOLD, TIMOTHY B, PETERSON, ERIK J · 2010 to 2014
$1.6M
NIAID NIH HHS L30 AI071651NIAMS NIH HHS R01 AR057781NIAMS NIH HHS R01 AR060861NIAMS NIH HHS R01 AR065964
6 · The paper itself

Abstract

Type I interferon (IFN) is a primary pathogenic factor in systemic lupus erythematosus (SLE). Gain-of-function genetic variants in the type I IFN pathway have been associated with risk of disease. Common polygenic as well as rare monogenic influences on type I IFN have been demonstrated, supporting a complex genetic basis for high IFN in many SLE patients. Both SLE-associated autoantibodies and high type I IFN can be observed in the pre-disease state. Patients with SLE and evidence of high type I IFN have more active disease and a greater propensity to nephritis and other severe manifestations. Despite the well-established association between type I IFN and SLE, the specific triggers of type I IFN production, the mechanisms by which IFNs help perpetuate the cycle of autoreactive cells and autoantibody production are not completely clear. This review provides an updated overview of type I IFN in SLE pathogenesis, clinical manifestations, and current therapeutic strategies targeting this pathway.

Indexed as

HumansInterferon Type ILupus Erythematosus, SystemicInterferon Type I

Identifiers

PMID33246136
PMCPMC8054829
OpenAlexW3107031282

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.