Evidence map›Paper›PMID 39604413›Full record

ArticleScientific reports2024

Interleukin-17A is a potential therapeutic target predicted by proteomics for systemic sclerosis patients at high risk of pulmonary arterial hypertension.

Yuuichi Ono, Akira Mogami, Ryuta Saito, Noriyasu Seki, Sho Ishigaki, Hiroshi Takei, Keiko Yoshimoto, Kenji Chiba, Tsutomu Takeuchi, Yuko Kaneko

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Pulmonary Immune Cell Landscape Altered by Exposure to HIV,International journal of molecular sciences · 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

10 authors.

Yuuichi OnoSohyaku Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa, 227-0033, Japan.
Akira MogamiSohyaku Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa, 227-0033, Japan.
Ryuta SaitoSohyaku Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa, 227-0033, Japan.
Noriyasu SekiSohyaku Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa, 227-0033, Japan.
Sho IshigakiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Hiroshi TakeiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Keiko YoshimotoDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Kenji ChibaSohyaku Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa, 227-0033, Japan. Chiba.Kenji@mk.mt-pharma.co.jp.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, 160-8582, Japan.
Yuko KanekoDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, 160-8582, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We explored effective therapeutic targets for systemic sclerosis (SSc) patients with high risk for pulmonary arterial hypertension (PAH) by plasma proteomics analysis. A total of fifty-seven patients with SSc were enrolled in the study and the prevalence of PAH was 19.3%. On the other hand, 75.4% of SSc patients showed the ratio of forced vital capacity percentage/diffusing capacity of the lungs for carbon monoxide percentage> 1.6 and met criteria for high risk of PAH. Identification of elevated plasma proteins in SSc patients with high risk of PAH, followed by upstream regulator analysis, predicted interleukin (IL)-17A as a major upstream molecule. Furthermore, we performed in vitro neutralization study using MT-6194, a bispecific antibody targeting both IL-17A and IL-6 receptor. We found that MT-6194 broadly suppressed the increased expression of downstream molecules of IL-17A including IL-17A-related cytokines/chemokines, IL-17A-driven NFκB pathway and IL-6-driven JAK/STAT pathway which were shown to be increased in SSc patients with high risk of PAH by the proteomics. Consequently, it is revealed that IL-17A is a promising target for early intervention in SSc patients with high risk for PAH.

Indexed as

Interleukin-17ProteomicsScleroderma, SystemicAdultAgedFemaleHumansMaleMiddle AgedPulmonary Arterial HypertensionSignal TransductionIL17A protein, humanInterleukin-17

Identifiers

PMID39604413
PMCPMC11603215

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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.