Evidence map›Paper›PMID 27507062›Full record

ArticleScientific reports2016

Fine-mapping analysis revealed complex pleiotropic effect and tissue-specific regulatory mechanism of TNFSF15 in primary biliary cholangitis, Crohn's disease and leprosy.

Yonghu Sun, Astrid Irwanto, Licht Toyo-Oka, Myunghee Hong, Hong Liu, Anand Kumar Andiappan, Hyunchul Choi, Yuki Hitomi, Gongqi Yu, Yongxiang Yu and 18 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  5. [Research progress of autoantibodies in primary biliary cholangitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
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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

28 authors at 9 institutions in 4 countries.

Yonghu SunShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Astrid IrwantoHuman Genetics, Genome Institute of Singapore, Singapore 138672, Singapore.
Licht Toyo-OkaHuman Genetics, University of Tokyo, Graduate School of Medicine, Tokyo 113-0033, Japan.
Myunghee HongBiochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138736, Korea.
Hong LiuShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Anand Kumar AndiappanImmune Regulation, Singapore Immunology Network, Singapore 138648, Singapore.
Hyunchul ChoiBiochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138736, Korea.
Yuki HitomiHuman Genetics, University of Tokyo, Graduate School of Medicine, Tokyo 113-0033, Japan.
Gongqi YuShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Yongxiang YuShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Fangfang BaoShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Chuan WangShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Xian FuShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Zhenhua YueShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Honglei WangShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Huimin ZhangShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Minae KawashimaHuman Genetics, University of Tokyo, Graduate School of Medicine, Tokyo 113-0033, Japan.
Kaname KojimaIntegrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, 980-8573, Japan.
Masao NagasakiIntegrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, 980-8573, Japan.
Minoru NakamuraClinical Research Center, National Hospital Organization Nagasaki Medical Center, Onuma, Nagasaki 856-8562, Japan.
Suk-Kyun YangGastroenterology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138736, Korea.
Byong Duk YeGastroenterology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138736, Korea.
Yosua DeniseHuman Genetics, Genome Institute of Singapore, Singapore 138672, Singapore.
Olaf RotzschkeImmune Regulation, Singapore Immunology Network, Singapore 138648, Singapore.
Kyuyoung SongBiochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138736, Korea.
Katsushi TokunagaHuman Genetics, University of Tokyo, Graduate School of Medicine, Tokyo 113-0033, Japan.
Furen ZhangShandong Provincial Institute of Dermatology and Venereology, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Jianjun LiuHuman Genetics, Genome Institute of Singapore, Singapore 138672, Singapore.
Shandong Provincial Institute of Dermatology and Venereology · CNThe University of Tokyo · JPUlsan College · KRGenome Institute of Singapore · SGShandong First Medical University · CNSingapore Immunology Network · SGTohoku Medical Megabank Organization · JPNagasaki Medical Center · JPUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic polymorphism within the 9q32 locus is linked with increased risk of several diseases, including Crohn's disease (CD), primary biliary cholangitis (PBC) and leprosy. The most likely disease-causing gene within 9q32 is TNFSF15, which encodes the pro-inflammatory cytokine TNF super-family member 15, but it was unknown whether these disparate diseases were associated with the same genetic variance in 9q32, and how variance within this locus might contribute to pathology. Using genetic data from published studies on CD, PBC and leprosy we revealed that bearing a T allele at rs6478108/rs6478109 (r(2) = 1) or rs4979462 was significantly associated with increased risk of CD and decreased risk of leprosy, while the T allele at rs4979462 was associated with significantly increased risk of PBC. In vitro analyses showed that the rs6478109 genotype significantly affected TNFSF15 expression in cells from whole blood of controls, while functional annotation using publicly-available data revealed the broad cell type/tissue-specific regulatory potential of variance at rs6478109 or rs4979462. In summary, we provide evidence that variance within TNFSF15 has the potential to affect cytokine expression across a range of tissues and thereby contribute to protection from infectious diseases such as leprosy, while increasing the risk of immune-mediated diseases including CD and PBC.

Indexed as

Crohn DiseaseDatabases, GeneticFemaleGenetic Predisposition to DiseaseHumansLeprosyLiver Cirrhosis, BiliaryMaleOrgan SpecificityPolymorphism, Single NucleotideTumor Necrosis Factor Ligand Superfamily Member 15TNFSF15 protein, humanTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID27507062
PMCPMC4979016
OpenAlexW2501050146

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.