Evidence map›Paper›PMID 34642338›Full record

ArticleNature communications2021

Interleukin-31 promotes fibrosis and T helper 2 polarization in systemic sclerosis.

Ai Kuzumi, Ayumi Yoshizaki, Kazuki M Matsuda, Hirohito Kotani, Yuta Norimatsu, Maiko Fukayama, Satoshi Ebata, Takemichi Fukasawa, Asako Yoshizaki-Ogawa, Yoshihide Asano and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
12.1field-weighted citation impact, top 1% 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, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  17. Effects of FAPCancer drug resistance (Alhambra, Calif.) · 2025
    Article
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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

15 authors at 4 institutions in 1 country.

Ai KuzumiDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-2261-7469
Ayumi YoshizakiDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ayuyoshi@me.com.ORCID 0000-0002-8194-9140
Kazuki M MatsudaDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-6755-8047
Hirohito KotaniDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuta NorimatsuDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Maiko FukayamaDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Satoshi EbataDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takemichi FukasawaDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Asako Yoshizaki-OgawaDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshihide AsanoDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kyojiro MorikawaDepartment of Applied Chemistry, Graduate School of Engineering, The University of Tokyo, Tokyo, Japan.
Yutaka KazoeDepartment of System Design Engineering, Faculty of Science and Technology, Keio University, Yokohama, Japan.
Kazuma MawatariDepartment of Applied Chemistry, Graduate School of Engineering, The University of Tokyo, Tokyo, Japan.
Takehiko KitamoriDepartment of Bioengineering, Graduate School of Engineering, The University of Tokyo, Tokyo, Japan.
Shinichi SatoDepartment of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. satos-der@h.u-tokyo.ac.jp.
The University of Tokyo · JPKeio University · JPMeisei University · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a chronic multisystem disorder characterized by fibrosis and autoimmunity. Interleukin (IL)-31 has been implicated in fibrosis and T helper (Th) 2 immune responses, both of which are characteristics of SSc. The exact role of IL-31 in SSc pathogenesis is unclear. Here we show the overexpression of IL-31 and IL-31 receptor A (IL-31RA) in dermal fibroblasts (DFs) from SSc patients. We elucidate the dual role of IL-31 in SSc, where IL-31 directly promotes collagen production in DFs and indirectly enhances Th2 immune responses by increasing pro-Th2 cytokine expression in DFs. Furthermore, blockade of IL-31 with anti-IL-31RA antibody significantly ameliorates fibrosis and Th2 polarization in a mouse model of SSc. Therefore, in addition to defining IL-31 as a mediator of fibrosis and Th2 immune responses in SSc, our study provides a rationale for targeting the IL-31/IL-31RA axis in the treatment of SSc.

Indexed as

AdultAgedAnimalsAntibodies, MonoclonalCollagen Type ICollagen Type I, alpha 1 ChainDisease Models, AnimalFemaleFibroblastsFibrosisGene Expression RegulationHumansInterleukin-13Interleukin-4Interleukin-6InterleukinsAntibodies, MonoclonalCollagen Type ICollagen Type I, alpha 1 ChainIL13 protein, humanIL31 protein, humanIL31RA protein, humanIL4 protein, humanIL6 protein, humanInterleukin-13Interleukin-4Interleukin-6InterleukinsProtein IsoformsReceptors, InterleukinSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID34642338
PMCPMC8511151
OpenAlexW3207014451

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.