ArticleGenes and immunity2011
FoxP3 interacts with linker histone H1.5 to modulate gene expression and program Treg cell activity.
Article in Genes and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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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
14 citing papers in PubMed, 33 citations in OpenAlex.
- The Importance of the Transcription Factor Foxp3 in the Development of Primary Immunodeficiencies.Journal of clinical medicine · 2022Review
- The missing linkGenes & development · 2021Review
- Linker histone H1.5 is an underestimated factor in differentiation and carcinogenesis.Environmental epigenetics · 2020Review
- Disruption of FOXP3-EZH2 Interaction Represents a Pathobiological Mechanism in Intestinal Inflammation.Cellular and molecular gastroenterology and hepatology · 2019Article
- Role of H1 linker histones in mammalian development and stem cell differentiation.Biochimica et biophysica acta · 2016Review
- Modulating DNA methylation in activated CD8+ T cells inhibits regulatory T cell-induced binding of Foxp3 to the CD8+ T Cell IL-2 promoter.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Regulatory T cells and immune regulation of allergic diseases: roles of IL-10 and TGF-β.Genes and immunity · 2014Review
- Deimination of linker histones links neutrophil extracellular trap release with autoantibodies in systemic autoimmunity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Mapping of six somatic linker histone H1 variants in human breast cancer cells uncovers specific features of H1.2.Nucleic acids research · 2014Article
- Searching for the Achilles Heel of FOXP3.Frontiers in oncology · 2013Review
- Genetic polymorphism in FOXP3 gene: imbalance in regulatory T-cell role and development of human diseases.Journal of genetics · 2013Review
- The linker histone plays a dual role during gametogenesis in Saccharomyces cerevisiae.Molecular and cellular biology · 2012Article
- Structural and biological features of FOXP3 dimerization relevant to regulatory T cell function.Cell reports · 2012Article
- Novel roles of Caenorhabditis elegans heterochromatin protein HP1 and linker histone in the regulation of innate immune gene expression.Molecular and cellular biology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The forkhead box transcription factor FoxP3 controls the development and function of CD4+CD25+ regulatory T (Treg) cell. FoxP3 modulates gene expression in Treg cells by multiple epigenetic mechanisms that are not clearly defined. We identified FoxP3-interacting proteins in human T cells by co-immunoprecipitation/MS. We discovered that FoxP3 interacted with linker histone H1.5 via the leucine zipper (LZ) domain. Two independent IPEX patient-derived single residue mutations in the LZ of FoxP3 both abrogated its interaction with H1.5. Functionally, FoxP3 and H1.5 cooperatively repressed interleukin-2 (IL-2) expression in human T cells; and silencing of H1.5 expression inhibited the ability of FoxP3 to suppress IL-2 expression. We show that FoxP3 specifically enhanced H1.5 association at the IL-2 promoter, but reduce its association at the CTLA4 promoter, correlated with higher or lower histone acetylation of the respective promoters. Finally, silencing of H1.5 expression in human Treg cells impaired the Treg function to suppress target T cells. We conclude that FoxP3 interacts with H1.5 to alter its binding to target genes to modulate their expression and to program Treg function.
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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.