Evidence map›Paper›PMID 25683200›Full record

ArticleClinical and experimental immunology2015

Specific overexpression of tumour necrosis factor-α-induced protein (TNFAIP)9 in CD14(+) CD16(-) monocytes in patients with rheumatoid arthritis: comparative analysis with TNFAIP3.

C Takai, I Matsumoto, A Inoue, N Umeda, Y Tanaka, Y Kurashima, Y Wada, I Narita, T Sumida

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Immune Dysregulation in Autism Spectrum Disorder: What Do We Know about It?International journal of molecular sciences · 2022
    Review
  4. Article
  5. Review
  6. 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

9 authors at 2 institutions in 1 country.

C TakaiDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
I MatsumotoDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
A InoueDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
N UmedaDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
Y TanakaDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
Y KurashimaDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
Y WadaDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medicine and Dental Sciences, Niigata, Japan.
I NaritaDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medicine and Dental Sciences, Niigata, Japan.
T SumidaDivision of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba.
University of Tsukuba · JPNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour necrosis factor (TNF)-α-induced proteins (TNFAIP)9 and TNFAIP3 play an important pathogenic role in murine arthritis. To clarify their pathophysiological roles in patients with rheumatoid arthritis (RA), we examined their expression and localization in peripheral blood mononuclear cells (PBMC). TNFAIP9 and TNFAIP3 mRNA expression was determined in PBMC of RA patients and healthy subjects (control). Flow cytometry was used to analyse the main TNFAIP9- and TNFAIP3-expressing cell populations. TNFAIP9 and TNFAIP3 mRNA expression levels were examined in vitro on CD14(+) cells stimulated with TNF-α and lipopolysaccharide (LPS). The expression levels of TNFAIP9 and TNFAIP3 mRNA were also measured before and 12 weeks after treatment with tocilizumab and abatacept. TNFAIP9 expression was significantly higher, while TNFAIP3 expression was lower in PBMC of RA (n=36) than the control (n=24) (each P < 0.05). TNFAIP9 was expressed on CD14(+) cells, especially in human leucocyte antigen D-related (HLA-DR)(+) CD14(bright) CD16(-) cells, while TNFAIP3 was expressed mainly on CD3(+) T cells. TNF-α and LPS induced TNFAIP9 and TNFAIP3 in human CD14(+) monocytes in vitro. Treatment with tocilizumab (n=13), but not abatacept (n=11), significantly reduced TNFAIP9 mRNA expression in PBMC, which was associated with reduction in the number of circulating CD14(bright) monocytes. The expression of TNFAIP9 in CD14(+) cells was specifically elevated in patients with RA, regulated by TNF-α and LPS, and suppressed by tocilizumab, while TNFAIP3 in PBMC showed different localization and induction patterns.

Indexed as

Gene ExpressionAdultAgedAntibodies, Monoclonal, HumanizedAntirheumatic AgentsArthritis, RheumatoidCase-Control StudiesDNA-Binding ProteinsFemaleHumansImmunophenotypingIntracellular Signaling Peptides and ProteinsLeukocytes, MononuclearLipopolysaccharide ReceptorsLipopolysaccharidesMaleAntibodies, Monoclonal, HumanizedAntirheumatic AgentsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsLipopolysaccharide ReceptorsLipopolysaccharidesMembrane ProteinsNuclear ProteinsOxidoreductasesReceptors, IgGRNA, MessengerSTEAP4 protein, humanTNFAIP3 protein, humantocilizumabTumor Necrosis Factor-alphaTumor Necrosis Factor alpha-Induced Protein 3monocytespathogenesisrheumatoid arthritisTNFAIP9TNF-α-induced proteins

Identifiers

PMID25683200
PMCPMC4449774
OpenAlexW1696348685

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.