Evidence map›Paper›PMID 38162658›Full record

ArticleFrontiers in immunology2023

IL-17A-driven psoriasis is critically dependent on IL-36 signaling.

Berenice Fischer, Tanja Kübelbeck, Antonia Kolb, Julia Ringen, Ari Waisman, Miriam Wittmann, Susanne Karbach, Stephan Marcus Kölsch, Daniela Kramer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 18 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

9 authors at 3 institutions in 1 country.

Berenice FischerDepartment of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Tanja KübelbeckDepartment of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Antonia KolbDepartment of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Julia RingenCenter for Cardiology- Cardiology I, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Ari WaismanInstitute of Molecular Medicine, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Miriam WittmannDepartment of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Susanne KarbachCenter for Cardiology- Cardiology I, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Stephan Marcus KölschBoehringer Ingelheim Pharma GmbH & Co. KG, Medical Affairs, Ingelheim am Rhein, Germany.
Daniela KramerDepartment of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEBoehringer Ingelheim (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plaque psoriasis is an autoinflammatory and autoimmune skin disease, affecting 1-3% of the population worldwide. Previously, high levels of IL-36 family cytokines were found in psoriatic skin lesions, thereby contributing to keratinocyte hyperproliferation and infiltration of immune cells such as neutrophils. While treatment with anti-IL36 receptor (IL36R) antibodies was recently approved for generalized pustular psoriasis (GPP), it remains unclear, if targeting the IL36R might also inhibit plaque psoriasis. Here we show that antibody-mediated inhibition of IL36R is sufficient to suppress imiquimod-induced psoriasis-like skin inflammation and represses the disease's development in a model that depends on IL-17A overexpression in the skin. Importantly, treatment with anti-IL36R antibodies inhibited skin inflammation and attenuated psoriasis-associated, systemic inflammation. This is possibly due to a widespread effect of IL36R inhibition, which not only suppresses pro-inflammatory gene expression in keratinocytes, but also the activation of other immune cells such as T-cells or dendritic cells. In conclusion, we propose that inhibition of the IL-36 signaling pathway might constitute an attractive, alternative approach for treating IL-17A-driven psoriasis and psoriasis-linked comorbidities.

Indexed as

DermatitisPsoriasisHumansInflammationInterleukin-17Signal TransductionSkinInterleukin-17anti-IL36RIL-17Aimiquimodkeratinocytespsoriasisspesolimabsystemic inflammation

Identifiers

PMID38162658
PMCPMC10754973
OpenAlexW4389570212

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Registered trials

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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.