Evidence map›Paper›PMID 38368767›Full record

ArticleJournal of autoimmunity2024

LIGHT signaling through LTβR and HVEM in keratinocytes promotes psoriasis and atopic dermatitis-like skin inflammation.

Rinkesh K Gupta, Daniela Salgado Figueroa, Kai Fung, Haruka Miki, Jacqueline Miller, Ferhat Ay, Michael Croft

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Rinkesh K GuptaCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA.
Daniela Salgado FigueroaCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA; Bioinformatics and Systems Biology Program, University of California San Diego, La Jolla, CA 92093, USA.
Kai FungBioinformatics Core, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA.
Haruka MikiCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA.
Jacqueline MillerCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA.
Ferhat AyCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA; Bioinformatics and Systems Biology Program, University of California San Diego, La Jolla, CA 92093, USA; Department of Pediatrics, University of California San Diego, La Jolla, CA, 92093, USA.
Michael CroftCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, 92037, USA; Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA. Electronic address: mick@lji.org.
La Jolla Institute for Immunology · US

Funding

Studying the function of human genetic variation in the light of 3D genome organizationR35GM128938 · NIGMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI Ferhat Ay · 2018 to 2026
$4.6M
TWEAK and Skin InflammationR01AR072640 · NIAMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 2018 to 2022
$2.0M
NIAMS NIH HHS R01 AR072640
6 · The paper itself

Abstract

Psoriasis (PS) and atopic dermatitis (AD) are common skin inflammatory diseases characterized by hyper-responsive keratinocytes. Although, some cytokines have been suggested to be specific for each disease, other cytokines might be central to both diseases. Here, we show that Tumor necrosis factor superfamily member 14 (TNFSF14), known as LIGHT, is required for experimental PS, similar to its requirement in experimental AD. Mice devoid of LIGHT, or deletion of either of its receptors, lymphotoxin β receptor (LTβR) and herpesvirus entry mediator (HVEM), in keratinocytes, were protected from developing imiquimod-induced psoriatic features, including epidermal thickening and hyperplasia, and expression of PS-related genes. Correspondingly, in single cell RNA-seq analysis of PS patient biopsies, LTβR transcripts were found strongly expressed with HVEM in keratinocytes, and LIGHT was upregulated in T cells. Similar transcript expression profiles were also seen in AD biopsies, and LTβR deletion in keratinocytes also protected mice from allergen-induced AD features. Moreover, in vitro, LIGHT upregulated a broad spectrum of genes in human keratinocytes that are clinical features of both PS and AD skin lesions. Our data suggest that agents blocking LIGHT activity might be useful for therapeutic intervention in PS as well as in AD.

Indexed as

Dermatitis, AtopicPsoriasisAnimalsCytokinesHumansInflammationKeratinocytesLymphotoxin beta ReceptorMiceReceptors, Tumor Necrosis Factor, Member 14Tumor Necrosis Factor Ligand Superfamily Member 14CytokinesLymphotoxin beta ReceptorReceptors, Tumor Necrosis Factor, Member 14Tumor Necrosis Factor Ligand Superfamily Member 14Atopic dermatitisKeratinocyteLIGHTPsoriasisSkin inflammationTNF superfamily

Identifiers

PMID38368767
PMCPMC12406946
OpenAlexW4391906393

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.