ArticleImmunology2006
Splice variants of human FOXP3 are functional inhibitors of human CD4+ T-cell activation.
Article in Immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- Review
- Regulatory T cells in the breast cancer tumor microenvironment: new mechanisms, potential therapeutic strategies and future perspectives.American journal of cancer research · 2026Review
- Reprogramming intratumoral TScience immunology · 2025Article
- Review
- A splice of life: the discovery, function, and clinical implications of FOXP3 isoforms in autoimmune disease.International immunology · 2024Review
- Metabolic regulation of forkhead box P3 alternative splicing isoforms and their impact on health and disease.Frontiers in immunology · 2023Review
- FOXP3 exon 2 controls TScience immunology · 2022Article
- Thymic origins of autoimmunity-lessons from inborn errors of immunity.Seminars in immunopathology · 2021Review
- The DEL-1/β3 integrin axis promotes regulatory T cell responses during inflammation resolution.The Journal of clinical investigation · 2020Article
- Bronchoalveolar Tregs are associated with duration of mechanical ventilation in acute respiratory distress syndrome.Journal of translational medicine · 2020Article
- Protein Kinase C Theta Modulates PCMT1 through hnRNPL to Regulate FOXP3 Stability in Regulatory T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- The Impact of Dietary Components on Regulatory T Cells and Disease.Frontiers in immunology · 2020Review
- An immunometabolic pathomechanism for chronic obstructive pulmonary disease.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Molecular Mechanisms Controlling Foxp3 Expression in Health and Autoimmunity: From Epigenetic to Post-translational Regulation.Frontiers in immunology · 2019Review
- FoxP3 isoforms and PD-1 expression by T regulatory cells in multiple sclerosis.Scientific reports · 2018Article
- Clinical, Immunological, and Molecular Heterogeneity of 173 Patients With the Phenotype of Immune Dysregulation, Polyendocrinopathy, Enteropathy, X-Linked (IPEX) Syndrome.Frontiers in immunology · 2018Article
- Alternative Splicing of FOXP3-Virtue and Vice.Frontiers in immunology · 2018Review
- The regulation of immune tolerance by FOXP3.Nature reviews. Immunology · 2017Review
- Metabolic pressure and the breach of immunological self-tolerance.Nature immunology · 2017Article
- An expanded population of pathogenic regulatory T cells in giant cell arteritis is abrogated by IL-6 blockade therapy.Annals of the rheumatic diseases · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FOXP3 has been identified as a key regulator of immune homeostasis. Mutations within the FOXP3 gene result in dysregulated CD4+ T-cell function and elevated cytokine production, leading to lymphoproliferative disease. FOXP3 expression in CD4+ T cells is primarily detected with the CD4+ CD25+ regulatory T-cell population. In humans the protein is detected as a doublet following immunoblot analysis. The lower band of the doublet has been identified as a splice isoform lacking a region corresponding to exon 2. The aim of this study was to investigate whether the splice variant form lacking exon 2 and a new novel splice variant lacking both exons 2 and 7, were functional inhibitors of CD4+ T-cell activation. The data generated showed that full-length FOXP3 and both splice variant forms of the protein were functional repressors of CD4+ T-cell activation.
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Registered trials
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.