Evidence map›Paper›PMID 31819584›Full record

ArticleClinical, cosmetic and investigational dermatology2019

Interferon Kappa Is Up-Regulated in Psoriasis and It Up-Regulates Psoriasis-Associated Cytokines in vivo.

Yuanyuan Li, Yueqi Song, Leqing Zhu, Xiao Wang, Bin Yang, Ping Lu, Quan Chen, Lianghua Bin, Liehua Deng

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Clinical, cosmetic and investigational dermatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04242082 (Role of Glucose Transporter), which is not on this map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 32% 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.

NCT04242082 unknown statusnot on this mapstarted 2020, after this paper: background citation

Role of Glucose Transporter (GLUT) Genes Expression in Patients With Psoriasis

TypeobservationalSponsorAssiut UniversityRan2020 to 2021Enrolled75ConditionsPsoriasis VulgarisArmsGLUT 1 gene expression
3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation.The Journal of investigative dermatology · 2022
    Article
  5. Review
  6. Review
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 3 institutions in 2 countries.

Yuanyuan Li *Biomedical Translational Research Institute, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong Province, People's Republic of China.
Yueqi Song *Biomedical Translational Research Institute, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong Province, People's Republic of China.ORCID 0000-0002-7691-5288
Leqing Zhu *Biomedical Translational Research Institute, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong Province, People's Republic of China.
Xiao WangBiomedical Translational Research Institute, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong Province, People's Republic of China.
Bin YangDepartment of Dermatology, Dermatology Hospital of Southern Medical University, Guangzhou, Guangdong Province, People's Republic of China.ORCID 0000-0002-7155-6079
Ping LuDepartment of Dermatology, Dermatology Hospital of Southern Medical University, Guangzhou, Guangdong Province, People's Republic of China.ORCID 0000-0002-3787-4495
Quan ChenDivision of Research Informatics Services, Department of Medicine, National Jewish Health, Denver, CO, USA.
Lianghua BinDepartment of Pediatrics, National Jewish Health, Denver, CO, USA.ORCID 0000-0002-3786-0106
Liehua DengDepartment of Dermatology, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong Province, People's Republic of China.
First Affiliated Hospital of Jinan University · CNNational Jewish Health · USSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThere is increased type I interferon signature in psoriasis patients. Interferon-kappa (IFN-κ) is a member of type I interferon family that is constitutively expressed by keratinocytes. In this study, we investigate whether IFN-κ is involved in psoriasis etiology. PATIENTS AND

methodsTwenty healthy individuals, 20 psoriasis vulgaris patients and 10 atopic dermatitis (AD) were included for this study. Immunohistochemistry staining, normal human epidermal keratinocytes (NHEK) culture, Ca

resultsWe found IFN-κ protein expression was extremely low in the epidermis of normal skin, but it was significantly increased in the suprabasal layers of epidermal keratinocytes in psoriatic skin lesions. However, its expression in the skin lesions of AD was similar to normal skin. Additionally, IFN-κ protein was detected in sera from psoriasis patients, but not in sera from normal subjects and AD. We further investigated the regulation of

conclusionIncreased IFN-κ in psoriasis may be caused by injured cells-released nucleic acids, increased IFN-γ and self-activation. Its enhancement may contribute to the etiology of the disease by enhancing

Indexed as

atopic dermatitisIFN-κIL17ApsoriasisTNFA

Identifiers

PMID31819584
PMCPMC6890215
OpenAlexW2990848756

What OpenQuestion holds

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Registered trials

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.