Evidence map›Paper›PMID 32557263›Full record

ReviewClinical reviews in allergy & immunology2020

Type I Interferons in the Pathogenesis and Treatment of Autoimmune Diseases.

Jiao Jiang, Ming Zhao, Christopher Chang, Haijing Wu, Qianjin Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
14.9field-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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 158 citations in OpenAlex.

  1. Pooled it
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  6. Extracellular cGAMP in health and disease.Molecular biomedicine · 2026
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26 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

5 authors at 2 institutions in 2 countries.

Jiao JiangDepartment of Dermatology, Second Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China.
Ming ZhaoDepartment of Dermatology, Second Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China.
Christopher ChangDivision of Pediatric Immunology and Allergy, Joe DiMaggio Children's Hospital, Hollywood, FL, 33021, USA.
Haijing WuDepartment of Dermatology, Second Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China. chriswu1010@csu.edu.cn.
Qianjin LuDepartment of Dermatology, Second Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China. qianlu5860@csu.edu.cn.
Central South University · CNJoe DiMaggio Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFN-Is) are a very important group of cytokines that are produced by innate immune cells but also act on adaptive immune cells. IFN-Is possess antiviral, antitumor, and anti-proliferative effects, as well are associated with the initiation and maintenance of autoimmune disorders. Studies have shown that aberrantly expressed IFN-Is and/or type I IFN-inducible gene signatures in the serum or tissues of patients with autoimmune disorders are linked to their pathogenesis, clinical manifestations, and disease activity. Type I interferonopathies with mutations in genes impacting the type I IFN signaling pathway have shown symptoms and characteristics similar to those of systemic lupus erythematosus (SLE). Furthermore, both interventions in animal models and clinical trials of therapies targeting the type I IFN signaling pathway have shown efficacy in the treatment of autoimmune diseases. Our review aims to summarize the functions and targeted therapies (as well as clinical trials) of IFN-Is in both adult and pediatric autoimmune diseases, such as SLE, pediatric SLE (pSLE), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), juvenile dermatomyositis (JDM), Sjögren syndrome (SjS), and systemic sclerosis (SSc), discussing the potential abnormal regulation of transcription factors and epigenetic modifications and providing a potential mechanism for pathogenesis and therapeutic strategies for future clinical use.

Indexed as

Disease SusceptibilityAnimalsAutoimmune DiseasesBiomarkersCytokinesDisease ManagementEpigenesis, GeneticGene Expression RegulationGenetic Predisposition to DiseaseHumansInterferon Type IOrgan SpecificitySignal TransductionBiomarkersCytokinesInterferon Type IAutoimmune diseaseEpigenetic modificationsInterferonopathiesJuvenile idiopathic arthritisSjogren’s syndromeSystemic lupus erythematosusType I interferon signaling pathway

Identifiers

PMID32557263
OpenAlexW3036724399

What OpenQuestion holds

Textmetadata
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.