Evidence map›Paper›PMID 30042768›Full record

ArticleFrontiers in immunology2018

IL-1-IL-17 Signaling Axis Contributes to Fibrosis and Inflammation in Two Different Murine Models of Systemic Sclerosis.

Min-Jung Park, Su-Jin Moon, Eun-Jung Lee, Kyung-Ah Jung, Eun-Kyung Kim, Da-Som Kim, Jung-Ho Lee, Seung-Ki Kwok, Jun-Ki Min, Sung-Hwan Park and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

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  17. Treatable Traits in Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023
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4 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Min-Jung ParkThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Su-Jin MoonDivison of Rheumatology, Department of Internal Medicine, The Catholic University of Korea, Seoul, South Korea.
Eun-Jung LeeThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Kyung-Ah JungThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Eun-Kyung KimThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Da-Som KimThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Jung-Ho LeeDepartment of Plastic and Reconstructive Surgery, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Seung-Ki KwokDivison of Rheumatology, Department of Internal Medicine, The Catholic University of Korea, Seoul, South Korea.
Jun-Ki MinDivison of Rheumatology, Department of Internal Medicine, The Catholic University of Korea, Seoul, South Korea.
Sung-Hwan ParkDivison of Rheumatology, Department of Internal Medicine, The Catholic University of Korea, Seoul, South Korea.
Mi-La ChoThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSystemic sclerosis (SSc) is a progressive fibrotic disease that affects the skin and internal organs. Despite evidence implicating increased interleukin-17 (IL-17) activity in SSc, the role of IL-17 in SSc remains uncertain. The purpose of this study was to investigate whether IL-17 plays a pathophysiological role in SSc in two different murine models of SSc.

methodsBleomycin (BLM)-induced fibrosis and chronic graft-versus-host disease (cGVHD) models were used. Histological analysis was performed using Masson's trichrome and immunohistochemical staining. Quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunoassays were used to quantify the messenger RNA and protein levels of inflammatory mediators in dermal fibroblasts.

resultsIL-1 receptor antagonist-deficient (IL-1Ra-KO) mice were more severely affected by BLM injection, as shown by dermal and pulmonary fibrosis, compared with wild-type (WT) mice. Increased tissue fibrosis was reversed by knocking down IL-17.

conclusionTargeting IL-1 and its downstream IL-17 activity may be a novel treatment strategy for inhibiting inflammation and tissue fibrosis in SSc.

Indexed as

chronic graft-versus-host diseaseinterleukin-1interleukin-17lung fibrosisskin fibrosissystemic sclerosis

Identifiers

PMID30042768
PMCPMC6048384
OpenAlexW2810227809

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.