Evidence map›Paper›PMID 35883614›Full record

ArticleCells2022

Regulatory T Cells from Patients with Rheumatoid Arthritis Are Characterized by Reduced Expression of Ikaros Zinc Finger Transcription Factors.

Mara Dittrich-Salamon, Anja Meyer, Shuaifeng Yan, Eva Steinbach-Knödgen, Konstantin Kotschenreuther, David Stahl, Carola Tho Pesch, Joanna Schiller, Franziska Byrtus, Dorothee Jochimsen and 2 more

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

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  6. The 'TNature reviews. Rheumatology · 2025
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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

12 authors at 1 institution in 1 country.

Mara Dittrich-SalamonLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Anja MeyerLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.ORCID 0000-0001-9904-5070
Shuaifeng YanLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Eva Steinbach-KnödgenLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Konstantin KotschenreutherLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.ORCID 0000-0001-9455-2444
David StahlDivision of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Carola Tho PeschDivision of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Joanna SchillerDivision of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Franziska ByrtusDivision of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Dorothee JochimsenDivision of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
Viktoria Golumba-NagyLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.
David M KoflerLaboratory of Molecular Immunology, Division of Rheumatology and Clinical Immunology, Department I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpenerstr. 62, 50937 Cologne, Germany.ORCID 0000-0001-6164-3980
University of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T (Treg) cells play an important role in immune tolerance and contribute to the prevention of autoimmune diseases, including rheumatoid arthritis (RA). The differentiation, function and stability of Treg cells is controlled by members of the Ikaros zinc finger transcription factor family. In this study, we aimed to reveal how the expression of Ikaros transcription factors is affected by disease activity in RA. Therefore, we analyzed the ex vivo expression of Ikaros, Helios, Aiolos and Eos in Treg cells, Th17 cells and Th1 cells from RA patients by flow cytometry. We found significantly reduced expression of Helios, Aiolos and Eos in Treg cells from RA patients as compared to healthy controls. Moreover, Helios and Aiolos levels correlated with disease activity, as assessed by DAS28-CRP. In addition, Ikaros, Helios and Aiolos were significantly downregulated in Th1 cells from RA patients, while no difference between healthy individuals and RA was observed in Th17 cells. In summary, Helios and Aiolos expression in Treg cells correlates with disease activity and the expression levels of Ikaros transcription factors are diminished in Treg cells from RA patients. This observation could explain the reduced stability of Treg cells in RA.

Indexed as

Arthritis, RheumatoidIkaros Transcription FactorHumansTh17 CellsT-Lymphocytes, RegulatoryZinc FingersIkaros Transcription FactorAiolosDAS28-CRPdisease activityEosHeliosIkarosregulatory T cellsrheumatoid arthritisTh17 cellsTh1 cells

Identifiers

PMID35883614
PMCPMC9316388
OpenAlexW4285038459

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.