Regulatory T cells and Foxp3.
TLDR
Regulatory T (Treg) cells play central role in regulation of immune responses to self‐antigens, allergens, and commensal microbiota as well as immune response to infectious agents and tumors.Abstract:
Regulatory T (Treg) cells play central role in regulation of immune responses to self-antigens, allergens, and commensal microbiota as well as immune responses to infectious agents and tumors. Transcriptional factor Foxp3 serves as a lineage specification factor of Treg cells. Paucity of Treg cells due to loss-of-function mutations of the Foxp3 gene is responsible for highly aggressive, fatal, systemic immune-mediated inflammatory lesions in mice and humans. Recent studies of Foxp3 expression and function provided critical novel insights into biology of Treg cells and into cellular mechanisms of the immune homeostasis.read more
Citations
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TL;DR: Understanding how epigenetic alterations and Foxp3 expression coordinately control Treg-cell-specific gene regulation will enable better control of immune responses by targeting the generation and maintenance of Treg cells.
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References
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Journal ArticleDOI
Control of Regulatory T Cell Development by the Transcription Factor Foxp3
TL;DR: Foxp3, which encodes a transcription factor that is genetically defective in an autoimmune and inflammatory syndrome in humans and mice, is specifically expressed in naturally arising CD4+ regulatory T cells and retroviral gene transfer of Foxp3 converts naïve T cells toward a regulatory T cell phenotype similar to that of naturally occurring CD4+.
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Foxp3 programs the development and function of CD4 + CD25 + regulatory T cells
TL;DR: It is reported that the forkhead transcription factor Foxp3 is specifically expressed in CD4+CD25+ regulatory T cells and is required for their development and function and ectopic expression ofFoxp3 confers suppressor function on peripheral CD4-CD25− T cells.
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Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.
TL;DR: The authors showed that CD4+CD25+ cells contribute to maintaining self-tolerance by downregulating immune response to self and non-self Ags in an Ag-nonspecific manner, presumably at the T cell activation stage.
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The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3.
Craig L. Bennett,Jacinda R. Christie,Fred Ramsdell,Mary E. Brunkow,Polly J. Ferguson,Luke Whitesell,Thaddeus E. Kelly,Frank T. Saulsbury,Phillip F. Chance,Hans D. Ochs +9 more
TL;DR: Genetic evidence is presented that different mutations of the human gene FOXP3, the ortholog of the gene mutated in scurfy mice (Foxp3), causes IPEX syndrome.
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An essential role for Scurfin in CD4+CD25+ T regulatory cells.
TL;DR: It is shown that Foxp3 is highly expressed by TR cells and is associated with TR cell activity and phenotype, indicating that the Scurfin and CTLA-4 pathways may intersect and providing further insight into the TR cell lineage.