Evidence map›Paper›PMID 34223817›Full record

ArticleeLife2021

Soluble Fas ligand drives autoantibody-induced arthritis by binding to DR5/TRAIL-R2.

Dongjin Jeong, Hye Sung Kim, Hye Young Kim, Min Jueng Kang, Hyeryeon Jung, Yumi Oh, Donghyun Kim, Jaemoon Koh, Sung-Yup Cho, Yoon Kyung Jeon and 6 more

Abstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
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

16 authors.

Dongjin Jeong *Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-7122-1220
Hye Sung Kim *Laboratory of Immune Regulation in Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0003-1297-7081
Hye Young KimDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-5978-512X
Min Jueng KangDepartment of Molecular Medicine and Biopharmaceutical Sciences, School of Convergence Science, Seoul, Republic of Korea.
Hyeryeon JungDepartment of Molecular Medicine and Biopharmaceutical Sciences, School of Convergence Science, Seoul, Republic of Korea.ORCID 0000-0001-5179-8604
Yumi OhDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Donghyun KimLaboratory of Immune Regulation in Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-7863-7384
Jaemoon KohDepartment of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Sung-Yup ChoDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, Republic of Korea.
Yoon Kyung JeonDepartment of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-8466-9681
Eun Bong LeeDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0003-0703-1208
Seung Hyo LeeGraduate School of Medical Science and Engineering, Korean Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Eui-Cheol ShinGraduate School of Medical Science and Engineering, Korean Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.ORCID 0000-0002-6308-9503
Ho Min KimGraduate School of Medical Science and Engineering, Korean Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.ORCID 0000-0003-0029-3643
Eugene C YiDepartment of Molecular Medicine and Biopharmaceutical Sciences, School of Convergence Science, Seoul, Republic of Korea.
Doo Hyun ChungDepartment of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-9948-8485

Funding

Ministry of Health and Welfare HI14C1277
6 · The paper itself

Abstract

To date, no study has demonstrated that soluble Fas ligand (sFasL)-mediated inflammation is regulated via interaction with Fas in vivo. We found that FasL interacts specifically with tumor necrosis factor receptor superfamily (TNFRSF)10B, also known as death receptor (DR)5. Autoantibody-induced arthritis (AIA) was attenuated in FasL (

Indexed as

AnimalsArthritisAutoantibodiesCell LineFas Ligand ProteinHumansJurkat CellsMiceReceptors, TNF-Related Apoptosis-Inducing LigandAutoantibodiesFas Ligand ProteinReceptors, TNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanTnfrsf10b protein, mousearthritisCX3CL1DR5humanimmunologyinflammationmedicinemousesoluble fas ligand

Identifiers

PMID34223817
PMCPMC8257255

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.