Evidence map›Paper›PMID 28522454›Full record

ArticleAnnals of the rheumatic diseases2017

Multiomic disease signatures converge to cytotoxic CD8 T cells in primary Sjögren's syndrome.

Shinya Tasaki, Katsuya Suzuki, Ayumi Nishikawa, Yoshiaki Kassai, Maiko Takiguchi, Rina Kurisu, Yuumi Okuzono, Takahiro Miyazaki, Masaru Takeshita, Keiko Yoshimoto and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Pooled it
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  9. Shared gene signatures between rheumatoid arthritis and Sjögren's syndrome.American journal of clinical and experimental immunology · 2026
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8 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

18 authors at 5 institutions in 2 countries.

Shinya TasakiIntegrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Katsuya SuzukiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Ayumi NishikawaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Yoshiaki KassaiImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Maiko TakiguchiImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Rina KurisuImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Yuumi OkuzonoImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Takahiro MiyazakiImmunology Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Masaru TakeshitaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Keiko YoshimotoDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Hidekata YasuokaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Kunihiro YamaokaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Kazuhiro IkeuraDepartment of Dentistry and Oral Surgery, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Kazuyuki TsunodaDepartment of Dentistry and Oral Surgery, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Rimpei MoritaDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Akihiko YoshimuraDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Hiroyoshi ToyoshibaIntegrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa City, Kanagawa, Japan.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Keio University · JPCenter for Rheumatology · USTakeda (Japan) · JPNektar Therapeutics (United States) · USRush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMultiomics study was conducted to elucidate the crucial molecular mechanisms of primary Sjögren's syndrome (SS) pathology.

methodsWe generated multiple data set from well-defined patients with SS, which includes whole-blood transcriptomes, serum proteomes and peripheral immunophenotyping. Based on our newly generated data, we performed an extensive bioinformatic investigation.

resultsOur integrative analysis identified SS gene signatures (SGS) dysregulated in widespread omics layers, including epigenomes, mRNAs and proteins. SGS predominantly involved the interferon signature and ADAMs substrates. Besides, SGS was significantly overlapped with SS-causing genes indicated by a genome-wide association study and expression trait loci analyses. Combining the molecular signatures with immunophenotypic profiles revealed that cytotoxic CD8 -T cells- were associated with SGS. Further, we observed the activation of SGS in cytotoxic CD8 T cells isolated from patients with SS.

conclusionsOur multiomics investigation identified gene signatures deeply associated with SS pathology and showed the involvement of cytotoxic CD8 T cells. These integrative relations across multiple layers will facilitate our understanding of SS at the system level.

Indexed as

EpigenomicsGene Expression ProfilingImmunophenotypingProteomicsADAM ProteinsAdultAgedCD8-Positive T-LymphocytesComputational BiologyFemaleGenome-Wide Association StudyHumansMaleMiddle AgedRNA, MessengerSjogren's SyndromeADAM ProteinsRNA, MessengerDisease ActivityGene PolymorphismSjgren's Syndrome

Identifiers

PMID28522454
PMCPMC5738597
OpenAlexW2616391641

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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.