ArticleScientific reports2017
Ectopic FOXP3 Expression Preserves Primitive Features Of Human Hematopoietic Stem Cells While Impairing Functional T Cell Differentiation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- T Cell Development and Responses in Human Immune System Mice.Annual review of immunology · 2025Review
- Harnessing the biology of regulatory T cells to treat disease.Nature reviews. Drug discovery · 2025Review
- Characterization of the MT-2 Treg-like cell line in the presence and absence of forkhead box P3 (FOXP3).Immunology and cell biology · 2024Article
- Article
- Correcting inborn errors of immunity: From viral mediated gene addition to gene editing.Seminars in immunology · 2023Review
- Rare immune diseases paving the road for genome editing-based precision medicine.Frontiers in genome editing · 2023Review
- Towards gene therapy for IPEX syndrome.European journal of immunology · 2022Review
- Modeling human T1D-associated autoimmune processes.Molecular metabolism · 2022Review
- Precise somatic genome editing for treatment of inborn errors of immunity.Frontiers in immunology · 2022Review
- Gene Therapy for Primary Immunodeficiency.HemaSphere · 2021Review
- CRISPR-based gene editing enablesScience advances · 2020Article
- Glioma-associated oncogene homolog 1 stimulates FOXP3 to promote non-small cell lung cancer stemness.American journal of translational research · 2020Article
- Gene therapy targeting haematopoietic stem cells for inherited diseases: progress and challenges.Nature reviews. Drug discovery · 2019Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FOXP3 is the transcription factor ruling regulatory T cell function and maintenance of peripheral immune tolerance, and mutations in its coding gene causes IPEX autoimmune syndrome. FOXP3 is also a cell-cycle inhibitor and onco-suppressor in different cell types. In this work, we investigate the effect of ectopic FOXP3 expression on HSC differentiation and we challenged this approach as a possible HSC-based gene therapy for IPEX. FOXP3-expressing HSC showed reduced proliferation ability and increased maintenance of primitive markers in vitro in both liquid and OP9-ΔL1 co-cultures. When transplanted into immunodeficient mice, FOXP3-expressing HSC showed significantly enhanced engraftment ability. This was due to a pronounced increase in the frequency of repopulating cells, as assessed by extreme limiting dilution assay. Likely underlying the increased repopulating ability, FOXP3 expressing HSC showed significantly enhanced expression of genes controlling stemness features. However, peripheral T cells developed in the FOXP3-humanized mice were quantitatively reduced and hyporesponsive to cytokine and polyclonal stimulation. Our findings reveal unpredicted effects of FOXP3 in the biology of HSC and may provide new tools to manipulate primitive features in HSC for clinical applications. Moreover, they formally prove the need of preserving endogenous FOXP3 regulation for an HSC-based gene therapy approach for IPEX syndrome.
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