Evidence map›Paper›PMID 31167762›Full record

ArticleAnnals of the rheumatic diseases2019

Multi-dimensional analysis identified rheumatoid arthritis-driving pathway in human T cell.

Masaru Takeshita, Katsuya Suzuki, Yasushi Kondo, Rimpei Morita, Yuumi Okuzono, Keiko Koga, Yoshiaki Kassai, Kanae Gamo, Maiko Takiguchi, Rina Kurisu and 4 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 91 citations in OpenAlex.

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  2. Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026
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  14. Resolution of inflammation during rheumatoid arthritis.Frontiers in cell and developmental biology · 2025
    Review
  15. Article
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  17. Article
  18. Article
  19. Durable CD4Trends in immunology · 2024
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Masaru TakeshitaDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.ORCID 0000-0002-3281-6595
Katsuya SuzukiDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.
Yasushi KondoDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.
Rimpei MoritaDepartment of Microbiology and Immunology, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.
Yuumi OkuzonoResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Keiko KogaResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Yoshiaki KassaiResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Kanae GamoResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Maiko TakiguchiResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Rina KurisuResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Hideyuki MototaniResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Yukihiko EbisunoResearch, Immunology Unit, Takeda Pharmaceutical Co Ltd, Fujisawa-Shi, Kanagawa, Japan.
Akihiko YoshimuraDepartment of Microbiology and Immunology, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan tsutake@z5.keio.jp.
Takeda (Japan) · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRheumatoid arthritis (RA) is an autoimmune disease accompanied by lymphocyte infiltration into joint synovium. While T cells are considered to be important for its pathogenesis, the features that are the most relevant to disease and how they change after treatment remain unclear. The aim of this study was to clarify the characteristics of T cells in RA, comprehensively.

methodsWe enrolled a total of 311 patients with RA and 73 healthy participants, and carefully classified them by disease state, constructed multiple cohorts and analysed clinical samples from them in a stepwise manner. We performed immunophenotyping with multiple evaluation axes, and two independent transcriptome analyses complementary to each other.

resultsWe identified that 'effector memory-Tfh' subset was specifically expanded in the peripheral blood (PB) of patients with RA in correlation with disease activity, and reverted after treatment. Besides, we revealed distinct features of T cells in synovial fluid (SF) that the expression of Tfh/Tph-related genes and pro-inflammatory cytokines and chemokines, including

conclusionOur multi-dimensional investigation identified disease relevant T-cell subsets and gene signatures deeply involved in pathogenesis of RA. These findings could aid in our understanding of essential roles of T cells in RA and will facilitate to development better diagnostic and therapeutic interventions.

Indexed as

AdultArthritis, RheumatoidChemokine CXCL13CytokinesFemaleHumansImmunophenotypingMaleMiddle AgedSignal TransductionSynovial FluidT-Lymphocyte SubsetsChemokine CXCL13CXCL13 protein, humanCytokinesrheumatoid arthritissynovial fluidT cell

Identifiers

PMID31167762
PMCPMC6788883
OpenAlexW2956066087

What OpenQuestion holds

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Registered trials

None linked

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.