Evidence map›Paper›PMID 40568113›Full record

ArticlebioRxiv : the preprint server for biology2025

Preserved suppressive function despite loss of Foxp3: insights into the identity of regulatory T cells.

B Luckerbauer, A V Villarino, A Laurence, K Hirahara, G Sciume, Y Mikami, H Y Shih, H W Sun, A Tosevska, M Brinkmann and 5 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

B LuckerbauerMedical University of Vienna, Division of Rheumatology, Department of Internal Medicine 3, Vienna, Austria.
A V VillarinoDepartment of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
A LaurenceTranslational Gastroenterology Unit, Department of Haematology, University College Hospital, UCLH Hospitals NHS Trust, University of Oxford, Oxford, UK.
K HiraharaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
G SciumeDepartment of Molecular Medicine, Sapienza University of Rome, Rome 00161, Italy.
Y MikamiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
H Y ShihNeuro-Immune Regulome Unit, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA; National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
H W SunBiodata Mining and Discovery Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
A TosevskaMedical University of Vienna, Division of Rheumatology, Department of Internal Medicine 3, Vienna, Austria.
M BrinkmannMedical University of Vienna, Division of Rheumatology, Department of Internal Medicine 3, Vienna, Austria.
S R BrooksNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.
J ScheffelDermatological Allergology, Allergie-Centrum-Charité, Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
F MeylanOffice of Science and Technology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, NIH, Bethesda, MD 20892, United States.
B AfzaliImmunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
M BonelliMedical University of Vienna, Division of Rheumatology, Department of Internal Medicine 3, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T (Treg) cells are essential for maintaining immune homeostasis, with Foxp3 acting as the master transcription factor governing their differentiation and function. The acquisition of effector signatures in Treg cells is closely tied to the surrounding tissue-specific immune environment and typically occurs alongside Foxp3 expression. In this study, we investigated the transcriptomic and functional consequences of Treg-mediated regulation in a Th2-driven disease setting. The application of both

Identifiers

PMID40568113
PMCPMC12190763

What OpenQuestion holds

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Registered trials

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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.