Evidence map›Paper›PMID 33344483›Full record

ArticleFrontiers in medicine2020

Foxp3-Positive Regulatory T Cells Contribute to Antifibrotic Effects in Renal Fibrosis via an Interleukin-18 Receptor Signaling Pathway.

Yasuaki Hirooka, Yuji Nozaki, Kaoru Niki, Asuka Inoue, Masafumi Sugiyama, Koji Kinoshita, Masanori Funauchi, Itaru Matsumura

Open access · goldAbstract read
In one paragraph

Article in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  5. Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022
    Review
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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

8 authors at 2 institutions in 1 country.

Yasuaki HirookaDepartment of Rheumatology, Kindai University Nara Hospital, Nara, Japan.
Yuji NozakiDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Kaoru NikiDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Asuka InoueDepartment of Rheumatology, Kindai University Nara Hospital, Nara, Japan.
Masafumi SugiyamaDepartment of Rheumatology, Kindai University Nara Hospital, Nara, Japan.
Koji KinoshitaDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Masanori FunauchiDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Itaru MatsumuraDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Kindai University · JPNara Medical University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal interstitial fibrosis is a common lesion in the process of various progressive renal diseases. Interleukin (IL)-18 is a proinflammatory cytokine that plays an important role in the induction of Th1 responses and is associated with renal interstitial fibrosis, but the mechanism of fibrosis remains unclear. Here we used IL-18 receptor alpha knockout (IL-18Rα KO) mice to investigate the role of an IL-18Rα signaling pathway in renal fibrosis in a murine model of unilateral ureteral obstruction. IL-18 Rα KO mice showed decreased renal interstitial fibrosis and increased infiltration of CD4+ T cells and Foxp3+ regulatory T cells (Tregs) compared to wildtype (WT) mice. The expression of renal transforming growth factor beta 1 (TGF-β1, which is considered an important cytokine in renal interstitial fibrosis) was not significantly different between WT and IL-18Rα KO mice. The adoptive transfer of CD4+ T cells from the splenocytes of IL-18Rα KO mice to WT mice reduced renal interstitial fibrosis and increased the number of Foxp3+ Tregs in WT mice. These results demonstrated that Foxp3+ Tregs have a protective effect in renal interstitial fibrosis via an IL-18R signaling pathway.

Indexed as

IL-18IL-18 receptorregulatory T cellsrenal fibrosisunilateral ureteral obstruction

Identifiers

PMID33344483
PMCPMC7738332
OpenAlexW3110422269

What OpenQuestion holds

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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.