Evidence map›Paper›PMID 31252033›Full record

ArticleThe Journal of investigative dermatology2020

IL-20-Receptor Signaling Delimits IL-17 Production in Psoriatic Inflammation.

Hye-Lin Ha, Hongshan Wang, Estefania Claudio, Wanhu Tang, Ulrich Siebenlist

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Psoriasis and Leprosy: An Arcane Relationship.Journal of inflammation research · 2023
    Article
  7. Article
  8. Article
  9. Psoriasis: Past, Present, and Future.The Journal of investigative dermatology · 2019
    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

5 authors at 1 institution in 1 country.

Hye-Lin HaImmune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Hongshan WangImmune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Estefania ClaudioImmune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Wanhu TangImmune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Ulrich SiebenlistImmune Activation Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Electronic address: usiebenlist@niaid.nih.gov.
National Institutes of Health · US

Funding

Functions of IL-17 Family Cytokines in Health and DiseaseZIAAI001095 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SIEBENLIST, ULRICH · 2009 to 2020
$9.7M
Signaling Mechanisms of IL-17 Family CytokinesZIAAI001096 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SIEBENLIST, ULRICH · 2009 to 2013
$2.6M
Intramural NIH HHS ZIA AI001095Intramural NIH HHS ZIA AI001096
6 · The paper itself

Abstract

IL-17 cytokines, in particular IL-17A, are critical effectors in psoriasis. Antibodies that block IL-17A are highly efficacious in treating psoriasis. Likewise, disruption of IL-17 cytokines signaling, such as via the loss of the adaptor CIKS/Act1, ameliorates inflammation in mouse models of psoriasis. IL-17A promotes a cascade of effects, including the robust production of IL-19 in both humans and mice. IL-19, along with IL-20 and IL-24, signal via IL-20 receptors and comprise a subgroup within the IL-10 cytokine family. The role of these three cytokines in psoriasis is unresolved. They have been linked to inflammatory processes, including psoriatic pathology, but these cytokines have also been reported to suppress inflammation in other contexts. In this study, we demonstrate that signaling via IL-20 receptors, including in response to IL-19, delimited aspects of imiquimod-induced psoriatic inflammation. IL-20 receptor signaling suppressed the dermal production of the CCL2 chemokine and thereby reduced CCL-2-driven infiltration of inflammatory cells into the dermis, including IL-17A-producing γδT cells. This constitutes a negative feedback, since IL-17A strongly induces IL-19 in keratinocytes. The effects of IL-17 cytokines in this inflammatory setting are dynamic; they are central to the development of both dermal and epidermal hallmarks of psoriasis but also initiate a path to mitigate inflammatory damage.

Indexed as

AnimalsCell MovementChemokine CCL2DermisDisease Models, AnimalGene Expression RegulationHumansInflammationInterleukin-17InterleukinsMiceMice, Inbred C57BLMice, KnockoutPsoriasisReceptors, InterleukinSignal TransductionChemokine CCL2Il19 protein, mouseInterleukin-17interleukin-20 receptorInterleukinsReceptors, Interleukin

Identifiers

PMID31252033
PMCPMC6926146
OpenAlexW2954994223

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.