Evidence map›Paper›PMID 39740932›Full record

ArticleRMD open2024

Induction of interleukin 21 receptor expression via enhanced intracellular metabolism in B cells and its relevance to the disease activity in systemic lupus erythematosus.

Masanobu Ueno, Shigeru Iwata, Kaoru Yamagata, Yasuyuki Todoroki, Koshiro Sonomoto, Atsushi Nagayasu, Ippei Miyagawa, Satoshi Kubo, Yusuke Miyazaki, Hiroko Miyata and 4 more

Abstract read
In one paragraph

Article in RMD open, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
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  4. Review
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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

14 authors.

Masanobu UenoThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0009-0003-0212-172X
Shigeru IwataThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0000-0002-2076-1603
Kaoru YamagataThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Yasuyuki TodorokiThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Koshiro SonomotoThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0000-0002-4003-8842
Atsushi NagayasuThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Ippei MiyagawaThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Satoshi KuboThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0000-0001-9693-9263
Yusuke MiyazakiThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0000-0001-5692-3881
Hiroko MiyataThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Ryuichiro KandaThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.ORCID 0000-0001-8247-6595
Takafumi AritomiThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Shingo NakayamadaThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan.
Yoshiya TanakaThe First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan tanaka@med.uoeh-u.ac.jp.ORCID 0000-0002-0807-7139

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo elucidate the association between the changes in intracellular metabolism in the early stage of B cell activation and systemic lupus erythematosus (SLE) pathogenesis.

methodsCD19

resultsStimulation with CpG (Toll-like receptor 9 (TLR9) ligand) in vitro induced enhanced interleukin 21 (IL-21) receptor expression in CD19

conclusionIL-21R mRNA-GAPDH binding dissociation associated with rapid glycolytic enhancement by the TLR9 ligand in B cells may induce plasmocyte differentiation through IL-21 signals and be involved in exacerbating SLE.

Indexed as

B-LymphocytesLupus Erythematosus, SystemicReceptors, Interleukin-21AdultCase-Control StudiesCells, CulturedFemaleGene Expression RegulationGlycolysisHumansInterleukin-21InterleukinsLymphocyte ActivationMaleMiddle AgedRNA, MessengerInterleukin-21InterleukinsReceptors, Interleukin-21RNA, MessengerToll-Like Receptor 9Autoimmune DiseasesImmune System DiseasesLupus Erythematosus, Systemic

Identifiers

PMID39740932
PMCPMC11749818

What OpenQuestion holds

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LicenceCC BY-NC
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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.