Evidence map›Paper›PMID 34364883›Full record

ArticleThe Journal of investigative dermatology2022

IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation.

Mehrnaz Gharaee-Kermani, Shannon N Estadt, Lam C Tsoi, Sonya J Wolf-Fortune, Jianhua Liu, Xianying Xing, Jonathon Theros, Tamra J Reed, Lori Lowe, Dennis Gruszka and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-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

8 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Mehrnaz Gharaee-KermaniDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Department of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Shannon N EstadtDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Graduate Program in Immunology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Lam C TsoiDepartment of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Department of Computational Medicine and Bioinformatics, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Sonya J Wolf-FortuneDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Graduate Program in Immunology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Jianhua LiuDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Xianying XingDepartment of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Jonathon TherosDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Tamra J ReedDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Lori LoweDepartment of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Department of Pathology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Dennis GruszkaDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Department of Dermatology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Nicole L WardDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA; Department of Dermatology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Johann E GudjonssonDepartment of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
J Michelle KahlenbergDivision of Rheumatology, Department of Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA; Department of Dermatology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA. Electronic address: mkahlenb@med.umich.edu.
Michigan Medicine · USUniversity of Michigan · USCase Western Reserve University · US

Funding

University of Michigan Skin Biology and Diseases Resource-based CenterP30AR075043 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2019 to 2026
$6.6M
Psoriasis Center of Research TranslationP50AR070590 · NIAMS · CASE WESTERN RESERVE UNIVERSITY · PI CAMERON, MARK JAMES · 2017 to 2021
$6.5M
Role of the sex biased transcription factor VGLL3 in promoting autoimmune responses in SLER01AI130025 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2017 to 2026
$3.9M
Characterization of Interferon Kappa as a Novel Target in Cutaneous LupusR01AR071384 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Joanne Michelle Kahlenberg · 2017 to 2026
$3.6M
Kallikrein-PAR interactions in skin inflammationR01AR073196 · NIAMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WARD, NICOLE LEANNE · 2018 to 2023
$3.3M
Linking Disease Mechanisms and Outcomes in Rheumatic DiseasesK24AR076975 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Joanne Michelle Kahlenberg · 2020 to 2026
$910k
Role of the Psoriasis Associated IL23R Risk Variants on Th17 Biology and FunctionK08AR060802 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUDJONSSON, JOHANN ELI · 2011 to 2015
$636k
Determining the role of type I interferons in ultraviolet-B light induced keratinocyte deathF31AR077988 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOFTUS, SHANNON · 2020 to 2022
$109k
NIAID NIH HHS R01 AI130025NIAMS NIH HHS F31 AR077988NIAMS NIH HHS K08 AR060802NIAMS NIH HHS K24 AR076975NIAMS NIH HHS P30 AR075043NIAMS NIH HHS P50 AR070590NIAMS NIH HHS R01 AR071384NIAMS NIH HHS R01 AR073196
6 · The paper itself

Abstract

Psoriasis is a common, inflammatory autoimmune skin disease. Early detection of an IFN-1 signature occurs in many psoriasis lesions, but the source of IFN production remains debated. IFN-κ is an important source of IFN-1 production in the epidermis. We identified a correlation between IFN-regulated and psoriasis-associated genes in human lesional skin. We thus wanted to explore the effects of IFN-κ in psoriasis using the well-characterized imiquimod psoriasis model. Three mouse strains aged 10 weeks were used: wild-type C57Bl/6, C57Bl/6 that overexpress Ifnk in the epidermis (i.e., transgenic), and total body Ifnk

Indexed as

AnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalFemaleHumansImiquimodInflammationInterferon Type IMaleMiceMice, Inbred C57BLMice, KnockoutPsoriasisSkinCytokinesImiquimodinterferon kappaInterferon Type I

Identifiers

PMID34364883
PMCPMC8688309
OpenAlexW3191078884

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.