Evidence map›Paper›PMID 36049437›Full record

ArticleJournal of autoimmunity2022

Forced Fox-P3 expression can improve the safety and antigen-specific function of engineered regulatory T cells.

Jenny McGovern, Angelika Holler, Sharyn Thomas, Hans J Stauss

Open access · hybridAbstract read
In one paragraph

Article in Journal of autoimmunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Dual CD8 and TCR editing in regulatory T cells mediates HLA-A2-restricted tissue-specific homing.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  4. Review
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  12. Review
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  15. Molecular therapy. Methods & clinical development · 2023
    Article
  16. Synthetic Cell-Based Immunotherapies for Neurologic Diseases.Neurology(R) neuroimmunology & neuroinflammation · 2023
    Review
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

4 authors at 1 institution in 2 countries.

Jenny McGovernInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London, UK; Quell Therapeutics, 84 Wood Lane, London, UK.
Angelika HollerInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London, UK.
Sharyn ThomasInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London, UK.
Hans J StaussInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London, UK. Electronic address: h.stauss@ucl.ac.uk.
The Royal Free Hospital · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Regulatory T cells (Treg) are potent inhibitors of autoreactive T cells. The intracellular transcription factor FoxP3 controls the expression levels of a diverse set of genes and plays a critical role in programming functional Tregs. Although, antigen-specific Tregs are more potent than polyclonal Tregs in treating ongoing autoimmunity, phenotype plasticity associated with loss of FoxP3 expression in Tregs can lead to the conversion into antigen-specific effector T cells which might exacerbate autoimmune pathology. In this study, we designed a retroviral vector driving the expression of FoxP3 and a human HLA-DR-restricted TCR from the same promoter. Transduction of purified human Tregs revealed that all TCR-positive cells had elevated levels of FoxP3 expression, increased CD25 and CTLA4 expression and potent suppressive function. Elevated FoxP3 expression did not impair the in vitro expansion of engineered Tregs. Adoptive transfer into HLA-DR transgenic mice revealed that FoxP3+TCR engineered Tregs showed long-term persistence with stable FoxP3 and TCR expression. In contrast, adoptive transfer of Tregs engineered with TCR only resulted in the accumulation of TCR-positive, FoxP3-negative T cells which displayed antigen-specific effector function when stimulated with the TCR-recognised peptides. Our data indicate that forced expression of FoxP3 can prevent accumulation of antigen-specific effector T cells without impairing the engraftment and persistence of engineered Tregs.

Indexed as

AutoimmunityT-Lymphocytes, RegulatoryAdoptive TransferAnimalsForkhead Transcription FactorsHumansMiceMice, TransgenicReceptors, Antigen, T-CellForkhead Transcription FactorsReceptors, Antigen, T-Cell

Identifiers

PMID36049437
PMCPMC10570926
OpenAlexW4293439694

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.