ArticleLeukemia2008
Malignant Tregs express low molecular splice forms of FOXP3 in Sézary syndrome.
Article in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 86 citations in OpenAlex.
- Altered balance between self-reactive T helper (Th)17 cells and Th10 cells and between full-length forkhead box protein 3 (FoxP3) and FoxP3 splice variants in Hashimoto's thyroiditis.Clinical and experimental immunology · 2015Trial
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- SRSF3 determines TScience advances · 2026Article
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- Blockade of the Immune Checkpoint CD47 by TTI-621 Potentiates the Response to Anti-PD-L1 in Cutaneous T-Cell Lymphoma.The Journal of investigative dermatology · 2023Article
- Spatially Guided and Single Cell Tools to Map the Microenvironment in Cutaneous T-Cell Lymphoma.Cancers · 2023Review
- Single-cell analysis of Sézary syndrome reveals novel markers and shifting gene profiles associated with treatment.Blood advances · 2023Article
- Article
- FOXP3+ Atypical Cells in Poikilodermatous Mycosis Fungoides.Acta dermato-venereologica · 2022Article
- The Role of Tumor Microenvironment in the Pathogenesis of Sézary Syndrome.International journal of molecular sciences · 2022Review
- Mogamulizumab efficacy is underscored by its associated rash that mimics cutaneous T-cell lymphoma: a retrospective single-centre case series.The British journal of dermatology · 2022Article
- High Expression of IKZF2 in Malignant T Cells Promotes Disease Progression in Cutaneous T Cell Lymphoma.Acta dermato-venereologica · 2021Article
- Sequence determinants as key regulators in gene expression of T cells.Immunological reviews · 2021Review
- Staphylococcus aureus enterotoxins induce FOXP3 in neoplastic T cells in Sézary syndrome.Blood cancer journal · 2020Article
- Colorectal cancer cell-derived CCL20 recruits regulatory T cells to promote chemoresistance via FOXO1/CEBPB/NF-κB signaling.Journal for immunotherapy of cancer · 2019Article
- Single-Cell Profiling of Cutaneous T-Cell Lymphoma Reveals Underlying Heterogeneity Associated with Disease Progression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Highly cytotoxic natural killer cells are associated with poor prognosis in patients with cutaneous T-cell lymphoma.Blood advances · 2018Article
- Alternative Splicing of FOXP3-Virtue and Vice.Frontiers in immunology · 2018Review
- The role of regulatory T cells and genes involved in their differentiation in pathogenesis of selected inflammatory and neoplastic skin diseases. Part II: The Treg role in skin diseases pathogenesis.Postepy dermatologii i alergologii · 2017Review
- Malignant inflammation in cutaneous T-cell lymphoma-a hostile takeover.Seminars in immunopathology · 2017Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sézary syndrome (SS) is an aggressive variant of cutaneous T-cell lymphoma. During disease progression, immunodeficiency develops; however, the underlying molecular and cellular mechanisms are not fully understood. Here, we study the regulatory T cell (Treg) function and the expression of FOXP3 in SS. We demonstrate that malignant T cells in 8 of 15 patients stain positive with an anti-FOXP3 antibody. Western blotting analysis shows expression of two low molecular splice forms of FOXP3, but not of wild-type (wt) FOXP3. The malignant T cells produce interleukin-10 and TGF-beta and suppress the growth of non-malignant T cells. The Treg phenotype and the production of suppressive cytokines are driven by aberrant activation of Jak3 independent of the FOXP3 splice forms. In contrast to wt FOXP3, the low molecular splice forms of FOXP3 have no inhibitory effect on nuclear factor-kappaB (NF-kappaB) activity in reporter assays which is in keeping with a constitutive NF-kappaB activity in the malignant T cells. In conclusion, we show that the malignant T cells express low molecular splice forms of FOXP3 and function as Tregs. Furthermore, we provide evidence that FOXP3 splice forms are functionally different from wt FOXP3 and not involved in the execution of the suppressive function. Thus, this is the first description of FOXP3 splice forms in human disease.
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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.