Evidence map›Paper›PMID 37399470›Full record

ReviewThe Journal of rheumatology2023

Type I Interferons in Autoimmunity: Implications in Clinical Phenotypes and Treatment Response.

Ana Carolina Londe, Ruth Fernandez-Ruiz, Paulo Rogério Julio, Simone Appenzeller, Timothy B Niewold

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
11.4field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

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  19. Robust CD4medRxiv : the preprint server for health sciences · 2025
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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

5 authors at 3 institutions in 3 countries.

Ana Carolina LondeA.C. Londe, MSc, Autoimmunity Lab, and Graduate Program in Physiopathology, School of Medical Science, State University of Campinas, Campinas, São Paulo, Brazil.
Ruth Fernandez-RuizR. Fernandez-Ruiz, MD, Department of Medicine, Hospital for Special Surgery, New York, New York, USA.ORCID 0000-0003-0759-5222
Paulo Rogério JulioP. Rogério Julio, MSc, Autoimmunity Lab, and Graduate Program of Child and Adolescent Health, School of Medical Science, State University of Campinas, Campinas, São Paulo, Brazil.
Simone AppenzellerS. Appenzeller, MD, PhD, Autoimmunity Lab, and Rheumatology Unit, Department of Medicine, School of Medical Science, State University of Campinas, Campinas, São Paulo, Brazil.
Timothy B NiewoldT.B. Niewold, MD, Department of Medicine, Hospital for Special Surgery, New York, New York, USA. niewoldt@hss.edu.
Universidade Estadual de Campinas (UNICAMP) · BRHospital Fernández · ARHospital for Special Surgery · US

Funding

Functional consequences of intergenic autoimmune disease risk variantsR01AI164968 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI F. Yesim Demirci, Timothy B Niewold · 2023 to 2026
$3.4M
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
PNP deficiency and cytosolic DNA in lupus pathogenesisR21AI167271 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2021 to 2021
$254k
Tfh cells in Human MyositisR21AR078416 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2021 to 2021
$229k
NIAID NIH HHS L30 AI071651NIAID NIH HHS R01 AI164968NIAID NIH HHS R21 AI167271NIAMS NIH HHS R01 AR057781NIAMS NIH HHS R01 AR060861NIAMS NIH HHS R01 AR065964NIAMS NIH HHS R21 AR078416
6 · The paper itself

Abstract

Type I interferon (IFN-I) is thought to play a role in many systemic autoimmune diseases. IFN-I pathway activation is associated with pathogenic features, including the presence of autoantibodies and clinical phenotypes such as more severe disease with increased disease activity and damage. We will review the role and potential drivers of IFN-I dysregulation in 5 prototypic autoimmune diseases: systemic lupus erythematosus, dermatomyositis, rheumatoid arthritis, primary Sjögren syndrome, and systemic sclerosis. We will also discuss current therapeutic strategies that directly or indirectly target the IFN-I system.

Indexed as

Autoimmune DiseasesInterferon Type ILupus Erythematosus, SystemicAntibodiesAutoimmunityHumansInterferonsPhenotypeAntibodiesInterferonsInterferon Type IautoimmunityinterferonsmyositisSjögren syndromesystemic lupus erythematosus

Identifiers

PMID37399470
PMCPMC12841979
OpenAlexW4382797860

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.