Evidence map›Paper›PMID 29339444›Full record

ArticleThe Journal of experimental medicine2018

LIGHT-HVEM signaling in keratinocytes controls development of dermatitis.

Rana Herro, Jr-Wen Shui, Sonja Zahner, Daniel Sidler, Yuko Kawakami, Toshiaki Kawakami, Koji Tamada, Mitchell Kronenberg, Michael Croft

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. The Central Roles of Keratinocytes in Coordinating Skin Immunity.The Journal of investigative dermatology · 2024
    Review
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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 2 institutions in 2 countries.

Rana HerroDivision of Immune Regulation, La Jolla Institute for Allergy and Immunology, La Jolla, CA.
Jr-Wen ShuiDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA.ORCID 0000-0002-5243-3727
Sonja ZahnerDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA.ORCID 0000-0003-0208-6656
Daniel SidlerDivision of Immune Regulation, La Jolla Institute for Allergy and Immunology, La Jolla, CA.
Yuko KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA.ORCID 0000-0002-4703-350X
Toshiaki KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA.
Koji TamadaDepartment of Immunology, Yamaguchi University School of Medicine, Yamaguchi, Japan.
Mitchell KronenbergDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA.
Michael CroftDivision of Immune Regulation, La Jolla Institute for Allergy and Immunology, La Jolla, CA mick@lji.org.ORCID 0000-0002-6062-3635
La Jolla Institute for Immunology · USYamaguchi University · JP

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
Using polygenic scores to enhance both variant discovery, and understanding of functional consequences of genetic variation in IBD.P01DK046763 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI TARGAN, STEPHAN R. · 1992 to 2020
$31.1M
The role of LIGHT in Colitis PathogenesisR01AI061516 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2004 to 2015
$4.5M
HVEM: A TNF family receptor that influences mucosal immunity and the microbiomeU01AI125955 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2016 to 2020
$2.7M
Mast cell Stat5-regulatory pathway in atopic dermatitisR01AR064418 · NIAMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2014 to 2018
$1.9M
Interaction of histamine-releasing factor with immunoglobulins in asthmaR01HL124283 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2014 to 2017
$1.9M
TNF Family Members and Control of Fibrotic DiseaseR21AI100905 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 2012 to 2013
$465k
The role of HVEM in inflammation and T cell FunctionF32DK082249 · NIDDK · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI SHUI, JRWEN · 2008 to 2010
$127k
NHLBI NIH HHS R01 HL124283NIAID NIH HHS R01 AI061516NIAID NIH HHS R21 AI100905NIAID NIH HHS U01 AI125955NIAID NIH HHS U19 AI070535NIAMS NIH HHS R01 AR064418NIDDK NIH HHS F32 DK082249NIDDK NIH HHS P01 DK046763
6 · The paper itself

Abstract

Dermatitis is often associated with an allergic reaction characterized by excessive type 2 responses leading to epidermal acanthosis, hyperkeratosis, and dermal inflammation. Although factors like IL-4, IL-13, and thymic stromal lymphopoietin (TSLP) are thought to be instrumental for the development of this type of skin disorder, other cytokines may be critical. Here, we show that the tumor necrosis factor (TNF) superfamily protein LIGHT (homologous to lymphotoxin, exhibits inducible expression, and competes with HSV glycoprotein D for binding to HVEM, a receptor expressed on T lymphocytes) is required for experimental atopic dermatitis, and LIGHT directly controls keratinocyte hyperplasia, and production of periostin, a matricellular protein that contributes to the clinical features of atopic dermatitis as well as other skin diseases such as scleroderma. Mice with a conditional deletion of the LIGHT receptor HVEM (herpesvirus entry mediator) in keratinocytes phenocopied LIGHT-deficient mice in exhibiting reduced epidermal thickening and dermal collagen deposition in a model of atopic dermatitis driven by house dust mite allergen. LIGHT signaling through HVEM in human epidermal keratinocytes directly induced proliferation and periostin expression, and both keratinocyte-specific deletion of HVEM or antibody blocking of LIGHT-HVEM interactions after disease onset prevented expression of periostin and limited atopic dermatitis symptoms. Developing reagents that neutralize LIGHT-HVEM signaling might be useful for therapeutic intervention in skin diseases where periostin is a central feature.

Indexed as

AnimalsAntigens, DermatophagoidesCell Adhesion MoleculesCell ProliferationDermatitis, AtopicDisease Models, AnimalHEK293 CellsHumansKeratinocytesMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, Tumor Necrosis Factor, Member 14RNA, Small InterferingSignal TransductionAntigens, DermatophagoidesCell Adhesion MoleculesPOSTN protein, humanReceptors, Tumor Necrosis Factor, Member 14RNA, Small InterferingTNFRSF14 protein, humanTnfrsf14 protein, mouseTNFSF14 protein, humanTnfsf14 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 14

Identifiers

PMID29339444
PMCPMC5789407
OpenAlexW2783554853

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.