Evidence map›Paper›PMID 31481114›Full record

ArticleArthritis research & therapy2019

Interferon-α exacerbates neuropsychiatric phenotypes in lupus-prone mice.

Jing Zeng, Xinyu Meng, Ping Zhou, Zhihua Yin, Qinglian Xie, Hong Zou, Nan Shen, Zhizhong Ye, Yuanjia Tang

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
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  11. Animal Inflammation-Based Models of Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2023
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  12. Review
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  14. Disease Activity-Associated Alteration of mRNA mFrontiers in cell and developmental biology · 2020
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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

9 authors at 5 institutions in 2 countries.

Jing ZengShanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shan Dong Road (c), Shanghai, China.
Xinyu MengShanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shan Dong Road (c), Shanghai, China.
Ping ZhouShanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shan Dong Road (c), Shanghai, China.
Zhihua YinShenzhen Futian Hospital for Rheumatic Diseases, 22 Nong Lin Road, Shenzhen, China.
Qinglian XieShanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), University of Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, China.
Hong ZouShanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), University of Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, China.
Nan ShenShanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shan Dong Road (c), Shanghai, China. nanshensibs@gmail.com.
Zhizhong YeShenzhen Futian Hospital for Rheumatic Diseases, 22 Nong Lin Road, Shenzhen, China. yezhizhong@126.com.
Yuanjia TangShanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shan Dong Road (c), Shanghai, China. tangyuanjia028@163.com.ORCID 0000-0002-2044-5424
Shanghai Jiao Tong University · CNShanghai Institutes for Biological Sciences · CNCincinnati Children's Hospital Medical Center · USRenji Hospital · CNShenzhen Zhongshan Urological Hospital · CN

Funding

National Key Research and Development Program of China 2017YFC0909000National Natural Science Foundation of China No.31630021, and 81421001National Natural Science Foundation of China No. 81571576, 81871287
6 · The paper itself

Abstract

backgroundNeuropsychiatric systemic lupus erythaematosus (NP-SLE) is one of the major manifestations of lupus. However, the mechanisms involved in NP-SLE are still largely unknown. The abnormal activation of the type I IFN signalling pathway is involved in SLE pathogenesis and is linked to NP-SLE, but the effect of IFN-α on NP-SLE encephalopathy has not been systematically studied.

methodsAn intravenous injection of Adv-IFN-α (10 mice, 10 × 10

resultsIn this study, we performed a series of behavioural tests to assess the neuropsychiatric phenotypes of IFN-α-treated NZB/NZW F1 mice and found that these mice developed a series of mental disorders such as anxiety-like phenotypes, depression-like phenotypes, deficits in sociability and cognitive impairments, which mimic the neuropsychiatric manifestations of NP-SLE, with a consistent onset and progression.

conclusionsOur research verified that IFN-α plays a critical role in NP-SLE and provides a comprehensive NP-SLE mouse model for dissecting the mechanisms of NP-SLE and developing novel therapies for intervention.

Indexed as

AnimalsDisease Models, AnimalFemaleImmunologic FactorsInjections, IntravenousInterferon-alphaLupus Vasculitis, Central Nervous SystemMiceMice, Inbred NZBPhenotypeImmunologic FactorsInterferon-alphaAutoimmunityCytokinesLupusNeuropsychiatric SLE (NP-SLE)

Identifiers

PMID31481114
PMCPMC6724270
OpenAlexW2971905302

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.