Evidence map›Paper›PMID 31332204›Full record

ArticleNature communications2019

CD160 serves as a negative regulator of NKT cells in acute hepatic injury.

Tae-Jin Kim, Gayoung Park, Jeongmin Kim, Seon Ah Lim, Jiyoung Kim, Kyungtaek Im, Min Hwa Shin, Yang-Xin Fu, Maria-Luisa Del Rio, Jose-Ignacio Rodriguez-Barbosa and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Article
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  16. Article
  17. Review
  18. BTLA inhibition has a dominant role in theFrontiers in immunology · 2022
    Article
  19. Article
  20. Article
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.

Tae-Jin KimDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Gayoung ParkDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Jeongmin KimDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Seon Ah LimDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Jiyoung KimDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Kyungtaek ImDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Min Hwa ShinDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Yang-Xin FuDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.ORCID http://orcid.org/0000-0002-4809-825X
Maria-Luisa Del RioTransplantation Immunobiology Section, Institute of Biomedicine, University of Leon, Leon, 24071, Spain.
Jose-Ignacio Rodriguez-BarbosaTransplantation Immunobiology Section, Institute of Biomedicine, University of Leon, Leon, 24071, Spain.
Cassian YeeDepartment of Melanoma Medical Oncology and department of Immunology, UT MD Anderson Cancer Center, Houston, TX, 77054, USA.
Kyung-Suk SuhDepartment of Surgery, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Seong-Jin KimPrecision Medicine Research Center, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Gyeonggi-do, 16229, Republic of Korea.
Sang-Jun HaDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. sjha@yonsei.ac.kr.ORCID http://orcid.org/0000-0002-1192-6031
Kyung-Mi LeeDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul, 02841, Republic of Korea. kyunglee@korea.ac.kr.ORCID http://orcid.org/0000-0002-5378-9258

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD160 and BTLA both bind to herpes virus entry mediator. Although a negative regulatory function of BTLA in natural killer T (NKT) cell activation has been reported, whether CD160 is also involved is unclear. By analyzing CD160

Indexed as

AnimalsAntigens, CDChemical and Drug Induced Liver InjuryConcanavalin ACytokinesGalactosylceramidesGPI-Linked ProteinsLiverLymphocyte ActivationMice, Inbred C57BLMice, KnockoutNatural Killer T-CellsReceptors, ImmunologicReceptors, Tumor Necrosis Factor, Member 14Survival Analysisalpha-galactosylceramideAntigens, CDBTLA protein, mouseCd160 protein, mouseConcanavalin ACytokinesGalactosylceramidesGPI-Linked ProteinsReceptors, ImmunologicReceptors, Tumor Necrosis Factor, Member 14Tnfrsf14 protein, mouse

Identifiers

PMID31332204
PMCPMC6646315

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.