Evidence map›Paper›PMID 31474191›Full record

ArticleLupus2019

Anti-IFNAR treatment does not reverse neuropsychiatric disease in MRL/

M W Huang, A D Stock, E V Mike, L Herlitz, R Kolbeck, C Putterman

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Lupus, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

M W HuangDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
A D StockDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
E V MikeDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
L HerlitzDepartment of Pathology, Cleveland Clinic, Cleveland, OH, USA.
R KolbeckResearch and Early Development, Respiratory, Inflammation and Autoimmune, Biopharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA.
C PuttermanDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0002-3204-6068
Albert Einstein College of Medicine · USAstraZeneca (United States) · USCleveland Clinic · US

Funding

TRAINING PROGRAM IN CELLULAR &MOLEC. BIOLOGY &GENETICST32GM007491 · NIGMS · YESHIVA UNIVERSITY · PI QUERY, CHARLES C · 1985 to 2021
$17.0M
NIGMS NIH HHS T32 GM007491NIH Training Program in Cellular and Molecular Biology and Genetics T32 CM007491
6 · The paper itself

Abstract

objectiveMany systemic lupus erythematosus patients display a type I interferon (IFN) signature, and IFNα levels positively correlate with disease severity. Previous studies blocking the type I IFN pathway systemically in lupus models showed some beneficial effects. However, its effects on neuropsychiatric manifestations have yet to be carefully assessed, even though IFNα has been associated with induction of depression. Our aim was to investigate whether disrupting the type I IFN pathway would attenuate the development of murine neuropsychiatric lupus.

methodsFemale MRL/

resultsNo significant differences were seen between the anti-IFNAR- and control-treated mice when assessing for depression-like behavior or cognitive dysfunction, although anti-IFNAR antibody-treated mice displayed significant decreases in levels of IFN-stimulated genes. Anti-IFNAR treatment also did not significantly improve brain histology, cellular infiltration, or blood-brain barrier integrity.

conclusionsSurprisingly, our results showed no improvement in neuropsychiatric disease and suggest that the role of IFNAR signaling in the pathogenesis of neuropsychiatric lupus continues to need to be carefully assessed.

Indexed as

AnimalsAntibodiesBehavior, AnimalCognitive DysfunctionDepressionDisease Models, AnimalFemaleInterferon-alphaInterferon Type ILupus Erythematosus, SystemicLupus Vasculitis, Central Nervous SystemMiceMice, Inbred MRL lprReceptor, Interferon alpha-betaSeverity of Illness IndexAntibodiesIfnar1 protein, mouseInterferon-alphaInterferon Type IReceptor, Interferon alpha-betaDepressionIFNARneuropsychiatric lupustype I interferon signature

Identifiers

PMID31474191
PMCPMC7541038
OpenAlexW2970780658

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.