Evidence map›Paper›PMID 32427877›Full record

ArticleScientific reports2020

Skin expression of IL-23 drives the development of psoriasis and psoriatic arthritis in mice.

Lili Chen, Madhura Deshpande, Marcos Grisotto, Paola Smaldini, Roberto Garcia, Zhengxiang He, Percio S Gulko, Sergio A Lira, Glaucia C Furtado

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-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

38 citing papers in PubMed, 56 citations in OpenAlex.

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  7. Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. Proceedings of the 2Mediterranean journal of rheumatology · 2026
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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 1 country.

Lili Chen *Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Madhura Deshpande *Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Marcos GrisottoPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Paola SmaldiniPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Roberto GarciaDepartment of Pathology and Laboratory Medicine, Hospital for Special Surgery, New York, NY, USA.
Zhengxiang HePrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Percio S GulkoDivision of Rheumatology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Sergio A LiraPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. sergio.lira@mssm.edu.
Glaucia C FurtadoPrecision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. glaucia.furtado@mssm.edu.
Icahn School of Medicine at Mount Sinai · USHospital for Special Surgery · US

Funding

Mechanisms associated with flares and remission in colitisR01DK110352 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2017 to 2025
$5.1M
Molecular pathogenesis of intestinal serrated polypsR01CA161373 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2011 to 2020
$3.7M
Mechanisms associated with diet-induced colitisR01DK121009 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LIRA, SERGIO A. · 2020 to 2023
$2.4M
Magnesium and Arthritis PathogenesisR01AR073165 · NIAMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GULKO, PERCIO S · 2019 to 2023
$1.8M
NIAMS NIH HHS R01 AR073165NIDDK NIH HHS R01 DK110352
6 · The paper itself

Abstract

Psoriasis (PS) is a chronic skin inflammation. Up to 30% of the patients with PS develop psoriatic arthritis (PsA), a condition characterized by inflammatory arthritis that affects joints or entheses. Although there is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of both PS and PsA, it remains unclear whether IL-23-induced skin inflammation drives joint disease. Here, we show that mice expressing increased levels of IL-23 in the skin (K23 mice) develop a PS-like disease that is characterized by acanthosis, parakeratosis, hyperkeratosis, and inflammatory infiltrates in the dermis. Skin disease preceded development of PsA, including enthesitis, dactylitis, and bone destruction. The development of enthesitis and dactylitis was not due to high circulating levels of IL-23, as transgenic animals and controls had similar levels of this cytokine in circulation. IL-22, a downstream cytokine of IL-23, was highly increased in the serum of K23 mice. Although IL-22 deficiency did not affect skin disease development, IL-22 deficiency aggravated the PsA-like disease in K23 mice. Our results demonstrate a central role for skin expressed IL-23 in the initiation of PS and on pathogenic processes leading to PsA.

Indexed as

AnimalsArthritis, PsoriaticFemaleHumansInterleukin-22Interleukin-23InterleukinsMaleMicePsoriasisSkinInterleukin-22Interleukin-23Interleukins

Identifiers

PMID32427877
PMCPMC7237669
OpenAlexW3026464895

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.